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Erschienen in: Cancer and Metastasis Reviews 1/2023

21.02.2023

Regulation of dormancy during tumor dissemination: the role of the ECM

verfasst von: Ananya Mukherjee, Jose Javier Bravo-Cordero

Erschienen in: Cancer and Metastasis Reviews | Ausgabe 1/2023

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Abstract

The study of the metastatic cascade has revealed the complexity of the process and the multiple cellular states that disseminated cancer cells must go through. The tumor microenvironment and in particular the extracellular matrix (ECM) plays an important role in regulating the transition from invasion, dormancy to ultimately proliferation during the metastatic cascade. The time delay from primary tumor detection to metastatic growth is regulated by a molecular program that maintains disseminated tumor cells in a non-proliferative, quiescence state known as tumor cell dormancy. Identifying dormant cells and their niches in vivo and how they transition to the proliferative state is an active area of investigation, and novel approaches have been developed to track dormant cells during dissemination. In this review, we highlight the latest research on the invasive nature of disseminated tumor cells and their link to dormancy programs. We also discuss the role of the ECM in sustaining dormant niches at distant sites.
Literatur
2.
3.
Zurück zum Zitat Bravo-Cordero, J. J., Hodgson, L., & Condeelis, J. (2012). Directed cell invasion and migration during metastasis. Current Opinion in Cell Biology, 24, 277–283.PubMedCrossRef Bravo-Cordero, J. J., Hodgson, L., & Condeelis, J. (2012). Directed cell invasion and migration during metastasis. Current Opinion in Cell Biology, 24, 277–283.PubMedCrossRef
5.
Zurück zum Zitat Mondal, C., Di Martino, J. S., & Bravo-Cordero, J. J. (2021). Actin dynamics during tumor cell dissemination. International Review of Cell and Molecular Biology, 360, 65–98.PubMedCrossRef Mondal, C., Di Martino, J. S., & Bravo-Cordero, J. J. (2021). Actin dynamics during tumor cell dissemination. International Review of Cell and Molecular Biology, 360, 65–98.PubMedCrossRef
7.
Zurück zum Zitat Werner-Klein, M., et al. (2018). Genetic alterations driving metastatic colony formation are acquired outside of the primary tumour in melanoma. Nature Communications, 9, 595.PubMedPubMedCentralCrossRef Werner-Klein, M., et al. (2018). Genetic alterations driving metastatic colony formation are acquired outside of the primary tumour in melanoma. Nature Communications, 9, 595.PubMedPubMedCentralCrossRef
8.
Zurück zum Zitat Ray, A., et al. (2022). Stromal architecture directs early dissemination in pancreatic ductal adenocarcinoma. JCI Insight, 7. Ray, A., et al. (2022). Stromal architecture directs early dissemination in pancreatic ductal adenocarcinoma. JCI Insight, 7.
9.
10.
Zurück zum Zitat Wang, J., & Kim, S. K. (2003). Global analysis of dauer gene expression in Caenorhabditis elegans. Development, 130, 1621–1634.PubMedCrossRef Wang, J., & Kim, S. K. (2003). Global analysis of dauer gene expression in Caenorhabditis elegans. Development, 130, 1621–1634.PubMedCrossRef
11.
Zurück zum Zitat Koornneef, M., Bentsink, L., & Hilhorst, H. (2002). Seed dormancy and germination. Current Opinion in Plant Biology, 5, 33–36.PubMedCrossRef Koornneef, M., Bentsink, L., & Hilhorst, H. (2002). Seed dormancy and germination. Current Opinion in Plant Biology, 5, 33–36.PubMedCrossRef
12.
Zurück zum Zitat Willis, R. A. (1934). The spread of tumours in the human body. J. A. Churchill. Willis, R. A. (1934). The spread of tumours in the human body. J. A. Churchill.
15.
Zurück zum Zitat Bryant, T. (1902). An analysis of forty-six cases of cancer of the breast which have been operated upon and survived the operation from 5 to 32 years, with remarks upon the treatment of recurrent growths, including the disease of the second breast, operative and otherwise. British Medical Journal, 1, 1200–1203.PubMedPubMedCentralCrossRef Bryant, T. (1902). An analysis of forty-six cases of cancer of the breast which have been operated upon and survived the operation from 5 to 32 years, with remarks upon the treatment of recurrent growths, including the disease of the second breast, operative and otherwise. British Medical Journal, 1, 1200–1203.PubMedPubMedCentralCrossRef
16.
Zurück zum Zitat Ashley, D. J. (1965). On the incidence of carcinoma of the prostate. The Journal of Pathology and Bacteriology, 90, 217–224.PubMedCrossRef Ashley, D. J. (1965). On the incidence of carcinoma of the prostate. The Journal of Pathology and Bacteriology, 90, 217–224.PubMedCrossRef
17.
Zurück zum Zitat Mortensen, J. D., Woolner, L. B., & Bennett, W. A. (1955). Gross and microscopic findings in clinically normal thyroid glands. The Journal of Clinical Endocrinology and Metabolism, 15, 1270–1280.PubMedCrossRef Mortensen, J. D., Woolner, L. B., & Bennett, W. A. (1955). Gross and microscopic findings in clinically normal thyroid glands. The Journal of Clinical Endocrinology and Metabolism, 15, 1270–1280.PubMedCrossRef
18.
Zurück zum Zitat Beckwith, J. B., & Perrin, E. V. (1963). In situ neuroblastomas: A contribution to the natural history of neural crest tumors. The American Journal of Pathology, 43, 1089–1104.PubMedPubMedCentral Beckwith, J. B., & Perrin, E. V. (1963). In situ neuroblastomas: A contribution to the natural history of neural crest tumors. The American Journal of Pathology, 43, 1089–1104.PubMedPubMedCentral
19.
Zurück zum Zitat Holmgren, L., O’Reilly, M. S., & Folkman, J. (1995). Dormancy of micrometastases: Balanced proliferation and apoptosis in the presence of angiogenesis suppression. Nature Medicine, 1, 149–153.PubMedCrossRef Holmgren, L., O’Reilly, M. S., & Folkman, J. (1995). Dormancy of micrometastases: Balanced proliferation and apoptosis in the presence of angiogenesis suppression. Nature Medicine, 1, 149–153.PubMedCrossRef
20.
Zurück zum Zitat Townson, J. L., & Chambers, A. F. (2006). Dormancy of solitary metastatic cells. Cell Cycle, 5, 1744–1750.PubMedCrossRef Townson, J. L., & Chambers, A. F. (2006). Dormancy of solitary metastatic cells. Cell Cycle, 5, 1744–1750.PubMedCrossRef
21.
22.
Zurück zum Zitat Phan, T. G., & Croucher, P. I. (2020). The dormant cancer cell life cycle. Nature Reviews. Cancer, 20, 398–411.PubMedCrossRef Phan, T. G., & Croucher, P. I. (2020). The dormant cancer cell life cycle. Nature Reviews. Cancer, 20, 398–411.PubMedCrossRef
23.
Zurück zum Zitat Naumov, G. N., Folkman, J., & Straume, O. (2009). Tumor dormancy due to failure of angiogenesis: Role of the microenvironment. Clinical & Experimental Metastasis, 26, 51–60.CrossRef Naumov, G. N., Folkman, J., & Straume, O. (2009). Tumor dormancy due to failure of angiogenesis: Role of the microenvironment. Clinical & Experimental Metastasis, 26, 51–60.CrossRef
24.
Zurück zum Zitat Naumov, G. N., Akslen, L. A., & Folkman, J. (2006). Role of angiogenesis in human tumor dormancy: Animal models of the angiogenic switch. Cell Cycle, 5, 1779–1787.PubMedCrossRef Naumov, G. N., Akslen, L. A., & Folkman, J. (2006). Role of angiogenesis in human tumor dormancy: Animal models of the angiogenic switch. Cell Cycle, 5, 1779–1787.PubMedCrossRef
25.
Zurück zum Zitat Almog, N., et al. (2006). Prolonged dormancy of human liposarcoma is associated with impaired tumor angiogenesis. FASEB Journal, 20, 947–949.PubMedCrossRef Almog, N., et al. (2006). Prolonged dormancy of human liposarcoma is associated with impaired tumor angiogenesis. FASEB Journal, 20, 947–949.PubMedCrossRef
26.
Zurück zum Zitat Senft, D., & Ronai, Z. A. (2016). Immunogenic, cellular, and angiogenic drivers of tumor dormancy--A melanoma view. Pigment Cell & Melanoma Research, 29, 27–42.CrossRef Senft, D., & Ronai, Z. A. (2016). Immunogenic, cellular, and angiogenic drivers of tumor dormancy--A melanoma view. Pigment Cell & Melanoma Research, 29, 27–42.CrossRef
27.
Zurück zum Zitat Shchors, K., et al. (2006). The Myc-dependent angiogenic switch in tumors is mediated by interleukin 1beta. Genes & Development, 20, 2527–2538.CrossRef Shchors, K., et al. (2006). The Myc-dependent angiogenic switch in tumors is mediated by interleukin 1beta. Genes & Development, 20, 2527–2538.CrossRef
28.
Zurück zum Zitat Stockmann, C., Schadendorf, D., Klose, R., & Helfrich, I. (2014). The impact of the immune system on tumor: Angiogenesis and vascular remodeling. Frontiers in Oncology, 4, 69.PubMedPubMedCentralCrossRef Stockmann, C., Schadendorf, D., Klose, R., & Helfrich, I. (2014). The impact of the immune system on tumor: Angiogenesis and vascular remodeling. Frontiers in Oncology, 4, 69.PubMedPubMedCentralCrossRef
29.
Zurück zum Zitat Koebel, C. M., et al. (2007). Adaptive immunity maintains occult cancer in an equilibrium state. Nature, 450, 903–907.PubMedCrossRef Koebel, C. M., et al. (2007). Adaptive immunity maintains occult cancer in an equilibrium state. Nature, 450, 903–907.PubMedCrossRef
30.
Zurück zum Zitat Schaller, J., & Agudo, J. (2020). Metastatic colonization: Escaping immune surveillance. Cancers (Basel), 12. Schaller, J., & Agudo, J. (2020). Metastatic colonization: Escaping immune surveillance. Cancers (Basel), 12.
32.
Zurück zum Zitat Mohme, M., Riethdorf, S., & Pantel, K. (2017). Circulating and disseminated tumour cells - Mechanisms of immune surveillance and escape. Nature Reviews Clinical Oncology, 14, 155–167.PubMedCrossRef Mohme, M., Riethdorf, S., & Pantel, K. (2017). Circulating and disseminated tumour cells - Mechanisms of immune surveillance and escape. Nature Reviews Clinical Oncology, 14, 155–167.PubMedCrossRef
33.
Zurück zum Zitat Salmon, H., et al. (2016). Expansion and activation of CD103+dendritic cell progenitors at the tumor site enhances tumor responses to therapeutic PD-L1 and BRAF inhibition. Immunity, 44, 924–938.PubMedPubMedCentralCrossRef Salmon, H., et al. (2016). Expansion and activation of CD103+dendritic cell progenitors at the tumor site enhances tumor responses to therapeutic PD-L1 and BRAF inhibition. Immunity, 44, 924–938.PubMedPubMedCentralCrossRef
34.
Zurück zum Zitat Mahnke, Y. D., Schwendemann, J., Beckhove, P., & Schirrmacher, V. (2005). Maintenance of long-term tumour-specific T-cell memory by residual dormant tumour cells. Immunology, 115, 325–336.PubMedPubMedCentralCrossRef Mahnke, Y. D., Schwendemann, J., Beckhove, P., & Schirrmacher, V. (2005). Maintenance of long-term tumour-specific T-cell memory by residual dormant tumour cells. Immunology, 115, 325–336.PubMedPubMedCentralCrossRef
35.
Zurück zum Zitat Müller-Hermelink, N., et al. (2008). TNFR1 signaling and IFN-gamma signaling determine whether T cells induce tumor dormancy or promote multistage carcinogenesis. Cancer Cell, 13, 507–518.PubMedCrossRef Müller-Hermelink, N., et al. (2008). TNFR1 signaling and IFN-gamma signaling determine whether T cells induce tumor dormancy or promote multistage carcinogenesis. Cancer Cell, 13, 507–518.PubMedCrossRef
37.
Zurück zum Zitat Linde, N., Fluegen, G., & Aguirre-Ghiso, J. A. (2016). The relationship between dormant cancer cells and their microenvironment. Advances in Cancer Research, 132. Linde, N., Fluegen, G., & Aguirre-Ghiso, J. A. (2016). The relationship between dormant cancer cells and their microenvironment. Advances in Cancer Research, 132.
38.
Zurück zum Zitat Risson, E., Nobre, A. R., Maguer-Satta, V., & Aguirre-Ghiso, J. A. (2020). The current paradigm and challenges ahead for the dormancy of disseminated tumor cells. Nature Cancer, 1, 672–680.PubMedPubMedCentralCrossRef Risson, E., Nobre, A. R., Maguer-Satta, V., & Aguirre-Ghiso, J. A. (2020). The current paradigm and challenges ahead for the dormancy of disseminated tumor cells. Nature Cancer, 1, 672–680.PubMedPubMedCentralCrossRef
39.
Zurück zum Zitat Raviraj, V., et al. (2012). Dormant but migratory tumour cells in desmoplastic stroma of invasive ductal carcinomas. Clinical & Experimental Metastasis, 29, 273–292.CrossRef Raviraj, V., et al. (2012). Dormant but migratory tumour cells in desmoplastic stroma of invasive ductal carcinomas. Clinical & Experimental Metastasis, 29, 273–292.CrossRef
40.
Zurück zum Zitat Bayarmagnai, B., et al. (2019). Invadopodia-mediated ECM degradation is enhanced in the G1 phase of the cell cycle. Journal of Cell Science, 132. Bayarmagnai, B., et al. (2019). Invadopodia-mediated ECM degradation is enhanced in the G1 phase of the cell cycle. Journal of Cell Science, 132.
42.
45.
Zurück zum Zitat Borriello, L., et al. (2022). Primary tumor associated macrophages activate programs of invasion and dormancy in disseminating tumor cells. Nature Communications, 13, 626.PubMedPubMedCentralCrossRef Borriello, L., et al. (2022). Primary tumor associated macrophages activate programs of invasion and dormancy in disseminating tumor cells. Nature Communications, 13, 626.PubMedPubMedCentralCrossRef
46.
Zurück zum Zitat Harney, A. S., et al. (2015). Real-time imaging reveals local, transient vascular permeability, and tumor cell intravasation stimulated by TIE2hi macrophage-derived VEGFA. Cancer Discovery, 5, 932–943.PubMedPubMedCentralCrossRef Harney, A. S., et al. (2015). Real-time imaging reveals local, transient vascular permeability, and tumor cell intravasation stimulated by TIE2hi macrophage-derived VEGFA. Cancer Discovery, 5, 932–943.PubMedPubMedCentralCrossRef
47.
Zurück zum Zitat Pignatelli, J., et al. (2014). Invasive breast carcinoma cells from patients exhibit MenaINV- and macrophage-dependent transendothelial migration. Science Signaling, 7, ra112.PubMedPubMedCentralCrossRef Pignatelli, J., et al. (2014). Invasive breast carcinoma cells from patients exhibit MenaINV- and macrophage-dependent transendothelial migration. Science Signaling, 7, ra112.PubMedPubMedCentralCrossRef
48.
Zurück zum Zitat Rohan, T. E., et al. (2014). Tumor microenvironment of metastasis and risk of distant metastasis of breast cancer. Journal of the National Cancer Institute, 106. Rohan, T. E., et al. (2014). Tumor microenvironment of metastasis and risk of distant metastasis of breast cancer. Journal of the National Cancer Institute, 106.
49.
Zurück zum Zitat Mondal, C., et al. (2022). A proliferative to invasive switch is mediated by srGAP1 downregulation through the activation of TGF-β2 signaling. Cell Reports, 40, 111358.PubMedCrossRef Mondal, C., et al. (2022). A proliferative to invasive switch is mediated by srGAP1 downregulation through the activation of TGF-β2 signaling. Cell Reports, 40, 111358.PubMedCrossRef
50.
Zurück zum Zitat Kienast, Y., et al. (2010). Real-time imaging reveals the single steps of brain metastasis formation. Nature Medicine, 16, 116–122.PubMedCrossRef Kienast, Y., et al. (2010). Real-time imaging reveals the single steps of brain metastasis formation. Nature Medicine, 16, 116–122.PubMedCrossRef
53.
Zurück zum Zitat Hong, M. K. H., et al. (2015). Tracking the origins and drivers of subclonal metastatic expansion in prostate cancer. Nature Communications, 6, 6605.PubMedCrossRef Hong, M. K. H., et al. (2015). Tracking the origins and drivers of subclonal metastatic expansion in prostate cancer. Nature Communications, 6, 6605.PubMedCrossRef
54.
Zurück zum Zitat Krøigård, A. B., et al. (2017). Genomic analyses of breast cancer progression reveal distinct routes of metastasis emergence. Scientific Reports, 7, 43813.PubMedPubMedCentralCrossRef Krøigård, A. B., et al. (2017). Genomic analyses of breast cancer progression reveal distinct routes of metastasis emergence. Scientific Reports, 7, 43813.PubMedPubMedCentralCrossRef
55.
Zurück zum Zitat Schwarz, R. F., et al. (2015). Spatial and temporal heterogeneity in high-grade serous ovarian cancer: A phylogenetic analysis. PLoS Medicine, 12, e1001789.PubMedPubMedCentralCrossRef Schwarz, R. F., et al. (2015). Spatial and temporal heterogeneity in high-grade serous ovarian cancer: A phylogenetic analysis. PLoS Medicine, 12, e1001789.PubMedPubMedCentralCrossRef
56.
Zurück zum Zitat Hoover, H. C. J., & Ketcham, A. S. (1975). Metastasis of metastases. American Journal of Surgery, 130, 405–411.PubMedCrossRef Hoover, H. C. J., & Ketcham, A. S. (1975). Metastasis of metastases. American Journal of Surgery, 130, 405–411.PubMedCrossRef
57.
Zurück zum Zitat Hart, I. R., & Fidler, I. J. (1980). Role of organ selectivity in the determination of metastatic patterns of B16 melanoma. Cancer Research, 40, 2281–2287.PubMed Hart, I. R., & Fidler, I. J. (1980). Role of organ selectivity in the determination of metastatic patterns of B16 melanoma. Cancer Research, 40, 2281–2287.PubMed
58.
Zurück zum Zitat Strauss, D. C., & Thomas, J. M. (2010). Transmission of donor melanoma by organ transplantation. The Lancet Oncology, 11, 790–796.PubMedCrossRef Strauss, D. C., & Thomas, J. M. (2010). Transmission of donor melanoma by organ transplantation. The Lancet Oncology, 11, 790–796.PubMedCrossRef
59.
Zurück zum Zitat Stephens, J. K., et al. (2000). Fatal transfer of malignant melanoma from multiorgan donor to four allograft recipients. Transplantation, 70, 232–236.PubMed Stephens, J. K., et al. (2000). Fatal transfer of malignant melanoma from multiorgan donor to four allograft recipients. Transplantation, 70, 232–236.PubMed
60.
Zurück zum Zitat Borriello, L., Condeelis, J., Entenberg, D., & Oktay, M. H. (2021). Breast cancer cell re-dissemination from lung metastases-A mechanism for enhancing metastatic burden. Journal of Clinical Medicine, 10. Borriello, L., Condeelis, J., Entenberg, D., & Oktay, M. H. (2021). Breast cancer cell re-dissemination from lung metastases-A mechanism for enhancing metastatic burden. Journal of Clinical Medicine, 10.
61.
Zurück zum Zitat Condeelis, J. S., & Entenberg, D. (2020). Hematogenous dissemination of breast cancer cells from lymph nodes is mediated by tumor microenvironment of metastasis doorways. Frontiers in Oncology, 10, 1–9. Condeelis, J. S., & Entenberg, D. (2020). Hematogenous dissemination of breast cancer cells from lymph nodes is mediated by tumor microenvironment of metastasis doorways. Frontiers in Oncology, 10, 1–9.
62.
Zurück zum Zitat Pereira, E. R., et al. (2018). Lymph node metastases can invade local blood vessels, exit the node, and colonize distant organs in mice. Science, 359, 1403–1407.PubMedPubMedCentralCrossRef Pereira, E. R., et al. (2018). Lymph node metastases can invade local blood vessels, exit the node, and colonize distant organs in mice. Science, 359, 1403–1407.PubMedPubMedCentralCrossRef
63.
Zurück zum Zitat Brown, M., et al. (2018). Lymph node blood vessels provide exit routes for metastatic tumor cell dissemination in mice. Science, 359, 1408–1411.PubMedCrossRef Brown, M., et al. (2018). Lymph node blood vessels provide exit routes for metastatic tumor cell dissemination in mice. Science, 359, 1408–1411.PubMedCrossRef
65.
66.
67.
Zurück zum Zitat Baccelli, I., et al. (2013). Identification of a population of blood circulating tumor cells from breast cancer patients that initiates metastasis in a xenograft assay. Nature Biotechnology, 31, 539–544.PubMedCrossRef Baccelli, I., et al. (2013). Identification of a population of blood circulating tumor cells from breast cancer patients that initiates metastasis in a xenograft assay. Nature Biotechnology, 31, 539–544.PubMedCrossRef
68.
Zurück zum Zitat Nemec, S., & Kilian, K. A. (2021). Materials control of the epigenetics underlying cell plasticity. Nature Reviews Materials, 6, 69–83.CrossRef Nemec, S., & Kilian, K. A. (2021). Materials control of the epigenetics underlying cell plasticity. Nature Reviews Materials, 6, 69–83.CrossRef
69.
Zurück zum Zitat Dai, J., et al. (2022). Astrocytic laminin-211 drives disseminated breast tumor cell dormancy in brain. Nature Cancer, 3, 25–42.PubMedCrossRef Dai, J., et al. (2022). Astrocytic laminin-211 drives disseminated breast tumor cell dormancy in brain. Nature Cancer, 3, 25–42.PubMedCrossRef
70.
Zurück zum Zitat Nallanthighal, S., Heiserman, J. P., & Cheon, D.-J. (2019). The role of the extracellular matrix in cancer stemness. Frontiers in Cell and Development Biology, 7, 86.CrossRef Nallanthighal, S., Heiserman, J. P., & Cheon, D.-J. (2019). The role of the extracellular matrix in cancer stemness. Frontiers in Cell and Development Biology, 7, 86.CrossRef
71.
72.
Zurück zum Zitat Karamanos, N. K., et al. (2021). A guide to the composition and functions of the extracellular matrix. The FEBS Journal, 288, 6850–6912.PubMedCrossRef Karamanos, N. K., et al. (2021). A guide to the composition and functions of the extracellular matrix. The FEBS Journal, 288, 6850–6912.PubMedCrossRef
74.
Zurück zum Zitat Wolfenson, H., Yang, B., & Sheetz, M. P. (2019). Steps in mechanotransduction pathways that control cell morphology. Annual Review of Physiology, 81, 585–605.PubMedCrossRef Wolfenson, H., Yang, B., & Sheetz, M. P. (2019). Steps in mechanotransduction pathways that control cell morphology. Annual Review of Physiology, 81, 585–605.PubMedCrossRef
75.
Zurück zum Zitat Kechagia, J. Z., Ivaska, J., & Roca-Cusachs, P. (2019). Integrins as biomechanical sensors of the microenvironment. Nature Reviews. Molecular Cell Biology, 20, 457–473.PubMedCrossRef Kechagia, J. Z., Ivaska, J., & Roca-Cusachs, P. (2019). Integrins as biomechanical sensors of the microenvironment. Nature Reviews. Molecular Cell Biology, 20, 457–473.PubMedCrossRef
76.
Zurück zum Zitat Burridge, K., Monaghan-Benson, E., & Graham, D. M. (2019). Mechanotransduction: From the cell surface to the nucleus via RhoA. Philosophical Transactions of the Royal Society B, 374, 20180229.CrossRef Burridge, K., Monaghan-Benson, E., & Graham, D. M. (2019). Mechanotransduction: From the cell surface to the nucleus via RhoA. Philosophical Transactions of the Royal Society B, 374, 20180229.CrossRef
77.
Zurück zum Zitat Ohashi, K., Fujiwara, S., & Mizuno, K. (2017). Roles of the cytoskeleton, cell adhesion and rho signalling in mechanosensing and mechanotransduction. Journal of Biochemistry, 161, 245–254.PubMed Ohashi, K., Fujiwara, S., & Mizuno, K. (2017). Roles of the cytoskeleton, cell adhesion and rho signalling in mechanosensing and mechanotransduction. Journal of Biochemistry, 161, 245–254.PubMed
78.
79.
Zurück zum Zitat Wang, Y., & Xiao, B. (2018). The mechanosensitive Piezo1 channel: Structural features and molecular bases underlying its ion permeation and mechanotransduction. The Journal of Physiology, 596, 969–978.PubMedCrossRef Wang, Y., & Xiao, B. (2018). The mechanosensitive Piezo1 channel: Structural features and molecular bases underlying its ion permeation and mechanotransduction. The Journal of Physiology, 596, 969–978.PubMedCrossRef
80.
Zurück zum Zitat Geng, J., et al. (2020). A plug-and-latch mechanism for gating the mechanosensitive Piezo Channel. Neuron, 106, 438–451.e6.PubMedCrossRef Geng, J., et al. (2020). A plug-and-latch mechanism for gating the mechanosensitive Piezo Channel. Neuron, 106, 438–451.e6.PubMedCrossRef
82.
Zurück zum Zitat Pathak, M. M., et al. (2014). Stretch-activated ion channel Piezo1 directs lineage choice in human neural stem cells. Proceedings of the National Academy of Sciences of the United States of America, 111, 16148–16153.PubMedPubMedCentralCrossRef Pathak, M. M., et al. (2014). Stretch-activated ion channel Piezo1 directs lineage choice in human neural stem cells. Proceedings of the National Academy of Sciences of the United States of America, 111, 16148–16153.PubMedPubMedCentralCrossRef
83.
Zurück zum Zitat Sun, X., et al. (2021). Bone piezoelectricity-mimicking nanocomposite membranes enhance osteogenic differentiation of bone marrow mesenchymal stem cells by amplifying cell adhesion and actin cytoskeleton. Journal of Biomedical Nanotechnology, 17, 1058–1067.PubMedCrossRef Sun, X., et al. (2021). Bone piezoelectricity-mimicking nanocomposite membranes enhance osteogenic differentiation of bone marrow mesenchymal stem cells by amplifying cell adhesion and actin cytoskeleton. Journal of Biomedical Nanotechnology, 17, 1058–1067.PubMedCrossRef
84.
Zurück zum Zitat Wang, F., et al. (2017). Mechanosensitive ion channel Piezo2 is important for enterochromaffin cell response to mechanical forces. The Journal of Physiology, 595, 79–91.PubMedCrossRef Wang, F., et al. (2017). Mechanosensitive ion channel Piezo2 is important for enterochromaffin cell response to mechanical forces. The Journal of Physiology, 595, 79–91.PubMedCrossRef
85.
Zurück zum Zitat Lai, A., et al. (2022). Mechanosensing by Piezo1 and its implications for physiology and various pathologies. Biological Reviews of the Cambridge Philosophical Society, 97, 604–614.PubMedCrossRef Lai, A., et al. (2022). Mechanosensing by Piezo1 and its implications for physiology and various pathologies. Biological Reviews of the Cambridge Philosophical Society, 97, 604–614.PubMedCrossRef
86.
Zurück zum Zitat Wu, J., Lewis, A. H., & Grandl, J. (2017). Touch, tension, and transduction - The function and regulation of Piezo ion channels. Trends in Biochemical Sciences, 42, 57–71.PubMedCrossRef Wu, J., Lewis, A. H., & Grandl, J. (2017). Touch, tension, and transduction - The function and regulation of Piezo ion channels. Trends in Biochemical Sciences, 42, 57–71.PubMedCrossRef
87.
Zurück zum Zitat Kenmochi, M., et al. (2022). Involvement of mechano-sensitive Piezo1 channel in the differentiation of brown adipocytes. The Journal of Physiological Sciences, 72, 13.PubMedCrossRef Kenmochi, M., et al. (2022). Involvement of mechano-sensitive Piezo1 channel in the differentiation of brown adipocytes. The Journal of Physiological Sciences, 72, 13.PubMedCrossRef
88.
Zurück zum Zitat Wang, N., Tytell, J. D., & Ingber, D. E. (2009). Mechanotransduction at a distance: Mechanically coupling the extracellular matrix with the nucleus. Nature Reviews. Molecular Cell Biology, 10, 75–82.PubMedCrossRef Wang, N., Tytell, J. D., & Ingber, D. E. (2009). Mechanotransduction at a distance: Mechanically coupling the extracellular matrix with the nucleus. Nature Reviews. Molecular Cell Biology, 10, 75–82.PubMedCrossRef
89.
Zurück zum Zitat Bouzid, T., et al. (2019). The LINC complex, mechanotransduction, and mesenchymal stem cell function and fate. Journal of Biological Engineering, 13, 68.PubMedPubMedCentralCrossRef Bouzid, T., et al. (2019). The LINC complex, mechanotransduction, and mesenchymal stem cell function and fate. Journal of Biological Engineering, 13, 68.PubMedPubMedCentralCrossRef
90.
Zurück zum Zitat Kalukula, Y., Stephens, A. D., Lammerding, J., & Gabriele, S. (2022). Mechanics and functional consequences of nuclear deformations. Nature Reviews. Molecular Cell Biology, 23, 583–602.PubMedPubMedCentralCrossRef Kalukula, Y., Stephens, A. D., Lammerding, J., & Gabriele, S. (2022). Mechanics and functional consequences of nuclear deformations. Nature Reviews. Molecular Cell Biology, 23, 583–602.PubMedPubMedCentralCrossRef
91.
Zurück zum Zitat Hamouda, M. S., Labouesse, C., & Chalut, K. J. (2020). Nuclear mechanotransduction in stem cells. Current Opinion in Cell Biology, 64, 97–104.PubMedCrossRef Hamouda, M. S., Labouesse, C., & Chalut, K. J. (2020). Nuclear mechanotransduction in stem cells. Current Opinion in Cell Biology, 64, 97–104.PubMedCrossRef
92.
Zurück zum Zitat Alam, S. G., et al. (2016). The mammalian LINC complex regulates genome transcriptional responses to substrate rigidity. Scientific Reports, 6, 38063.PubMedPubMedCentralCrossRef Alam, S. G., et al. (2016). The mammalian LINC complex regulates genome transcriptional responses to substrate rigidity. Scientific Reports, 6, 38063.PubMedPubMedCentralCrossRef
93.
Zurück zum Zitat Chang, W., Worman, H. J., & Gundersen, G. G. (2015). Accessorizing and anchoring the LINC complex for multifunctionality. The Journal of Cell Biology, 208, 11–22.PubMedPubMedCentralCrossRef Chang, W., Worman, H. J., & Gundersen, G. G. (2015). Accessorizing and anchoring the LINC complex for multifunctionality. The Journal of Cell Biology, 208, 11–22.PubMedPubMedCentralCrossRef
94.
Zurück zum Zitat Sharili, A. S., & Connelly, J. T. (2014). Nucleocytoplasmic shuttling: A common theme in mechanotransduction. Biochemical Society Transactions, 42, 645–649.PubMedCrossRef Sharili, A. S., & Connelly, J. T. (2014). Nucleocytoplasmic shuttling: A common theme in mechanotransduction. Biochemical Society Transactions, 42, 645–649.PubMedCrossRef
95.
Zurück zum Zitat Kofler, M., & Kapus, A. (2021). Nucleocytoplasmic shuttling of the mechanosensitive transcription factors MRTF and YAP /TAZ. Methods in Molecular Biology, 2299, 197–216.PubMedCrossRef Kofler, M., & Kapus, A. (2021). Nucleocytoplasmic shuttling of the mechanosensitive transcription factors MRTF and YAP /TAZ. Methods in Molecular Biology, 2299, 197–216.PubMedCrossRef
96.
Zurück zum Zitat Jang, J.-W., Kim, M.-K., & Bae, S.-C. (2020). Reciprocal regulation of YAP/TAZ by the Hippo pathway and the Small GTPase pathway. Small GTPases, 11, 280–288.PubMedCrossRef Jang, J.-W., Kim, M.-K., & Bae, S.-C. (2020). Reciprocal regulation of YAP/TAZ by the Hippo pathway and the Small GTPase pathway. Small GTPases, 11, 280–288.PubMedCrossRef
97.
Zurück zum Zitat Miranda, M. Z., Lichner, Z., Szászi, K., & Kapus, A. (2021). MRTF: Basic biology and role in kidney disease. International Journal of Molecular Sciences, 22. Miranda, M. Z., Lichner, Z., Szászi, K., & Kapus, A. (2021). MRTF: Basic biology and role in kidney disease. International Journal of Molecular Sciences, 22.
98.
Zurück zum Zitat Shreberk-Shaked, M., & Oren, M. (2019). New insights into YAP/TAZ nucleo-cytoplasmic shuttling: New cancer therapeutic opportunities? Molecular Oncology, 13, 1335–1341.PubMedPubMedCentralCrossRef Shreberk-Shaked, M., & Oren, M. (2019). New insights into YAP/TAZ nucleo-cytoplasmic shuttling: New cancer therapeutic opportunities? Molecular Oncology, 13, 1335–1341.PubMedPubMedCentralCrossRef
99.
Zurück zum Zitat Speight, P., Kofler, M., Szászi, K., & Kapus, A. (2016). Context-dependent switch in chemo/mechanotransduction via multilevel crosstalk among cytoskeleton-regulated MRTF and TAZ and TGFβ-regulated Smad3. Nature Communications, 7, 11642.PubMedPubMedCentralCrossRef Speight, P., Kofler, M., Szászi, K., & Kapus, A. (2016). Context-dependent switch in chemo/mechanotransduction via multilevel crosstalk among cytoskeleton-regulated MRTF and TAZ and TGFβ-regulated Smad3. Nature Communications, 7, 11642.PubMedPubMedCentralCrossRef
100.
Zurück zum Zitat Er, E. E., et al. (2018). Pericyte-like spreading by disseminated cancer cells activates YAP and MRTF for metastatic colonization. Nature Cell Biology, 20, 966–978.PubMedPubMedCentralCrossRef Er, E. E., et al. (2018). Pericyte-like spreading by disseminated cancer cells activates YAP and MRTF for metastatic colonization. Nature Cell Biology, 20, 966–978.PubMedPubMedCentralCrossRef
101.
102.
Zurück zum Zitat Zabransky, D. J., Jaffee, E. M., & Weeraratna, A. T. (2022). Shared genetic and epigenetic changes link aging and cancer. Trends in Cell Biology, 32, 338–350.PubMedCrossRef Zabransky, D. J., Jaffee, E. M., & Weeraratna, A. T. (2022). Shared genetic and epigenetic changes link aging and cancer. Trends in Cell Biology, 32, 338–350.PubMedCrossRef
104.
105.
Zurück zum Zitat Dawson, M. A., & Kouzarides, T. (2012). Cancer epigenetics: From mechanism to therapy. Cell, 150, 12–27.PubMedCrossRef Dawson, M. A., & Kouzarides, T. (2012). Cancer epigenetics: From mechanism to therapy. Cell, 150, 12–27.PubMedCrossRef
106.
Zurück zum Zitat Stowers, R., & Chaudhuri, O. (2021). Epigenetic regulation of mechanotransduction. Nature Biomedical Engineering, 5, 8–10.PubMedCrossRef Stowers, R., & Chaudhuri, O. (2021). Epigenetic regulation of mechanotransduction. Nature Biomedical Engineering, 5, 8–10.PubMedCrossRef
107.
Zurück zum Zitat Stowers, R. S., et al. (2019). Matrix stiffness induces a tumorigenic phenotype in mammary epithelium through changes in chromatin accessibility. Nature Biomedical Engineering, 3, 1009–1019.PubMedPubMedCentralCrossRef Stowers, R. S., et al. (2019). Matrix stiffness induces a tumorigenic phenotype in mammary epithelium through changes in chromatin accessibility. Nature Biomedical Engineering, 3, 1009–1019.PubMedPubMedCentralCrossRef
108.
Zurück zum Zitat Jang, M., et al. (2021). Matrix stiffness epigenetically regulates the oncogenic activation of the Yes-associated protein in gastric cancer. Nature Biomedical Engineering, 5, 114–123.PubMedCrossRef Jang, M., et al. (2021). Matrix stiffness epigenetically regulates the oncogenic activation of the Yes-associated protein in gastric cancer. Nature Biomedical Engineering, 5, 114–123.PubMedCrossRef
109.
Zurück zum Zitat Gupta, V. K., & Chaudhuri, O. (2022). Mechanical regulation of cell-cycle progression and division. Trends in Cell Biology, 32, 773–785.PubMedCrossRef Gupta, V. K., & Chaudhuri, O. (2022). Mechanical regulation of cell-cycle progression and division. Trends in Cell Biology, 32, 773–785.PubMedCrossRef
110.
Zurück zum Zitat Sosa, M. S., et al. (2015). NR2F1 controls tumour cell dormancy via SOX9- and RARβ-driven quiescence programmes. Nature Communications, 6, 6170.PubMedCrossRef Sosa, M. S., et al. (2015). NR2F1 controls tumour cell dormancy via SOX9- and RARβ-driven quiescence programmes. Nature Communications, 6, 6170.PubMedCrossRef
111.
Zurück zum Zitat Singh, D. K., et al. (2021). Epigenetic reprogramming of DCCs into dormancy suppresses metastasis <em>via</em> restored TGFβ–SMAD4 signaling. https://arxiv.org/abs/2021.08.01.454684. https://doi.org/10.1101/2021.08.01.454684 Singh, D. K., et al. (2021). Epigenetic reprogramming of DCCs into dormancy suppresses metastasis <em>via</em> restored TGFβ–SMAD4 signaling. https://​arxiv.​org/​abs/​2021.​08.​01.​454684.​ https://​doi.​org/​10.​1101/​2021.​08.​01.​454684
113.
Zurück zum Zitat Schofield, R. (1978). The relationship between the spleen colony-forming cell and the haemopoietic stem cell. Blood Cells, 4, 7–25.PubMed Schofield, R. (1978). The relationship between the spleen colony-forming cell and the haemopoietic stem cell. Blood Cells, 4, 7–25.PubMed
115.
Zurück zum Zitat Naba, A., et al. (2012). The matrisome: In silico definition and in vivo characterization by proteomics of normal and tumor extracellular matrices. Molecular & Cellular Proteomics, 11, M111.014647-M111.014647.CrossRef Naba, A., et al. (2012). The matrisome: In silico definition and in vivo characterization by proteomics of normal and tumor extracellular matrices. Molecular & Cellular Proteomics, 11, M111.014647-M111.014647.CrossRef
116.
Zurück zum Zitat Hynes, R. O., & Naba, A. (2012). Overview of the matrisome--An inventory of extracellular matrix constituents and functions. Cold Spring Harbor Perspectives in Biology, 4, a004903.PubMedPubMedCentralCrossRef Hynes, R. O., & Naba, A. (2012). Overview of the matrisome--An inventory of extracellular matrix constituents and functions. Cold Spring Harbor Perspectives in Biology, 4, a004903.PubMedPubMedCentralCrossRef
118.
Zurück zum Zitat Aguirre Ghiso, J. A., Kovalski, K., & Ossowski, L. (1999). Tumor dormancy induced by downregulation of urokinase receptor in human carcinoma involves integrin and MAPK signaling. The Journal of Cell Biology, 147, 89–103.PubMedCrossRef Aguirre Ghiso, J. A., Kovalski, K., & Ossowski, L. (1999). Tumor dormancy induced by downregulation of urokinase receptor in human carcinoma involves integrin and MAPK signaling. The Journal of Cell Biology, 147, 89–103.PubMedCrossRef
119.
Zurück zum Zitat Di Martino, J. S., et al. (2022). A tumor-derived type III collagen-rich ECM niche regulates tumor cell dormancy. Nature Cancer, 3, 90–107.PubMedCrossRef Di Martino, J. S., et al. (2022). A tumor-derived type III collagen-rich ECM niche regulates tumor cell dormancy. Nature Cancer, 3, 90–107.PubMedCrossRef
120.
Zurück zum Zitat Montagner, M., et al. (2020). Crosstalk with lung epithelial cells regulates Sfrp2-mediated latency in breast cancer dissemination. Nature Cell Biology, 22, 289–296.PubMedPubMedCentralCrossRef Montagner, M., et al. (2020). Crosstalk with lung epithelial cells regulates Sfrp2-mediated latency in breast cancer dissemination. Nature Cell Biology, 22, 289–296.PubMedPubMedCentralCrossRef
122.
Zurück zum Zitat Aouad, P., et al. (2022). Epithelial-mesenchymal plasticity determines estrogen receptor positive breast cancer dormancy and epithelial reconversion drives recurrence. Nature Communications, 13, 4975.PubMedPubMedCentralCrossRef Aouad, P., et al. (2022). Epithelial-mesenchymal plasticity determines estrogen receptor positive breast cancer dormancy and epithelial reconversion drives recurrence. Nature Communications, 13, 4975.PubMedPubMedCentralCrossRef
123.
Zurück zum Zitat Coppock, D. L., Kopman, C., Scandalis, S., & Gilleran, S. (1993). Preferential gene expression in quiescent human lung fibroblasts. Cell Growth and Differentiation, 4, 483–493.PubMed Coppock, D. L., Kopman, C., Scandalis, S., & Gilleran, S. (1993). Preferential gene expression in quiescent human lung fibroblasts. Cell Growth and Differentiation, 4, 483–493.PubMed
124.
Zurück zum Zitat Barkan, D., et al. (2010). Metastatic growth from dormant cells induced by a Col-I-enriched fibrotic environment. Cancer Research, 70, 5706–5716.PubMedPubMedCentralCrossRef Barkan, D., et al. (2010). Metastatic growth from dormant cells induced by a Col-I-enriched fibrotic environment. Cancer Research, 70, 5706–5716.PubMedPubMedCentralCrossRef
125.
Zurück zum Zitat Ohta, Y., et al. (2022). Cell-matrix interface regulates dormancy in human colon cancer stem cells. Nature, 608, 784–794.PubMedCrossRef Ohta, Y., et al. (2022). Cell-matrix interface regulates dormancy in human colon cancer stem cells. Nature, 608, 784–794.PubMedCrossRef
126.
Zurück zum Zitat Albrengues, J., et al. (2018). Neutrophil extracellular traps produced during inflammation awaken dormant cancer cells in mice. Science, 361(6409), eaao4227.PubMedPubMedCentralCrossRef Albrengues, J., et al. (2018). Neutrophil extracellular traps produced during inflammation awaken dormant cancer cells in mice. Science, 361(6409), eaao4227.PubMedPubMedCentralCrossRef
129.
Zurück zum Zitat Elkholi, I. E., Lalonde, A., Park, M., & Côté, J.-F. (2022). Breast cancer metastatic dormancy and relapse: An enigma of microenvironment(s). Cancer Research, 82, 4497–4510.PubMedPubMedCentralCrossRef Elkholi, I. E., Lalonde, A., Park, M., & Côté, J.-F. (2022). Breast cancer metastatic dormancy and relapse: An enigma of microenvironment(s). Cancer Research, 82, 4497–4510.PubMedPubMedCentralCrossRef
130.
Zurück zum Zitat Sosa, M. S., Bragado, P., & Aguirre-Ghiso, J. A. (2014). Mechanisms of disseminated cancer cell dormancy: An awakening field. Nature Reviews Cancer, 14, 611–622.PubMedPubMedCentralCrossRef Sosa, M. S., Bragado, P., & Aguirre-Ghiso, J. A. (2014). Mechanisms of disseminated cancer cell dormancy: An awakening field. Nature Reviews Cancer, 14, 611–622.PubMedPubMedCentralCrossRef
131.
Zurück zum Zitat Russo, S., Scotto di Carlo, F., & Gianfrancesco, F. (2022). The osteoclast traces the route to bone tumors and metastases. Frontiers in Cell and Development Biology, 10, 886305.CrossRef Russo, S., Scotto di Carlo, F., & Gianfrancesco, F. (2022). The osteoclast traces the route to bone tumors and metastases. Frontiers in Cell and Development Biology, 10, 886305.CrossRef
132.
Zurück zum Zitat Heyn, C., et al. (2006). In vivo MRI of cancer cell fate at the single-cell level in a mouse model of breast cancer metastasis to the brain. Magnetic Resonance in Medicine, 56, 1001–1010.PubMedCrossRef Heyn, C., et al. (2006). In vivo MRI of cancer cell fate at the single-cell level in a mouse model of breast cancer metastasis to the brain. Magnetic Resonance in Medicine, 56, 1001–1010.PubMedCrossRef
133.
Zurück zum Zitat Heyn, C., et al. (2006). In vivo magnetic resonance imaging of single cells in mouse brain with optical validation. Magnetic Resonance in Medicine, 55, 23–29.PubMedCrossRef Heyn, C., et al. (2006). In vivo magnetic resonance imaging of single cells in mouse brain with optical validation. Magnetic Resonance in Medicine, 55, 23–29.PubMedCrossRef
134.
Zurück zum Zitat Shapiro, E. M., Sharer, K., Skrtic, S., & Koretsky, A. P. (2006). In vivo detection of single cells by MRI. Magnetic Resonance in Medicine, 55, 242–249.PubMedCrossRef Shapiro, E. M., Sharer, K., Skrtic, S., & Koretsky, A. P. (2006). In vivo detection of single cells by MRI. Magnetic Resonance in Medicine, 55, 242–249.PubMedCrossRef
135.
136.
Zurück zum Zitat Fukumura, D., Duda, D. G., Munn, L. L., & Jain, R. K. (2010). Tumor microvasculature and microenvironment: Novel insights through intravital imaging in pre-clinical models. Microcirculation, 17, 206–225.PubMedPubMedCentralCrossRef Fukumura, D., Duda, D. G., Munn, L. L., & Jain, R. K. (2010). Tumor microvasculature and microenvironment: Novel insights through intravital imaging in pre-clinical models. Microcirculation, 17, 206–225.PubMedPubMedCentralCrossRef
137.
138.
Zurück zum Zitat Moore, N., & Lyle, S. (2011). Quiescent, slow-cycling stem cell populations in cancer: A review of the evidence and discussion of significance. Journal of Oncology, 2011. Moore, N., & Lyle, S. (2011). Quiescent, slow-cycling stem cell populations in cancer: A review of the evidence and discussion of significance. Journal of Oncology, 2011.
139.
Zurück zum Zitat Cotsarelis, G., Sun, T. T., & Lavker, R. M. (1990). Label-retaining cells reside in the bulge area of pilosebaceous unit: Implications for follicular stem cells, hair cycle, and skin carcinogenesis. Cell, 61, 1329–1337.PubMedCrossRef Cotsarelis, G., Sun, T. T., & Lavker, R. M. (1990). Label-retaining cells reside in the bulge area of pilosebaceous unit: Implications for follicular stem cells, hair cycle, and skin carcinogenesis. Cell, 61, 1329–1337.PubMedCrossRef
140.
Zurück zum Zitat Potten, C. S., Kellett, M., Roberts, S. A., Rew, D. A., & Wilson, G. D. (1992). Measurement of in vivo proliferation in human colorectal mucosa using bromodeoxyuridine. Gut, 33, 71–78.PubMedPubMedCentralCrossRef Potten, C. S., Kellett, M., Roberts, S. A., Rew, D. A., & Wilson, G. D. (1992). Measurement of in vivo proliferation in human colorectal mucosa using bromodeoxyuridine. Gut, 33, 71–78.PubMedPubMedCentralCrossRef
141.
Zurück zum Zitat Schillert, A., Trumpp, A., & Sprick, M. R. (2013). Label retaining cells in cancer--The dormant root of evil? Cancer Letters, 341, 73–79.PubMedCrossRef Schillert, A., Trumpp, A., & Sprick, M. R. (2013). Label retaining cells in cancer--The dormant root of evil? Cancer Letters, 341, 73–79.PubMedCrossRef
142.
Zurück zum Zitat Aguirre-Ghiso, J. A., Ossowski, L., & Rosenbaum, S. K. (2004). Green fluorescent protein tagging of extracellular signal-regulated kinase and p38 pathways reveals novel dynamics of pathway activation during primary and metastatic growth. Cancer Research, 64, 7336–7345.PubMedCrossRef Aguirre-Ghiso, J. A., Ossowski, L., & Rosenbaum, S. K. (2004). Green fluorescent protein tagging of extracellular signal-regulated kinase and p38 pathways reveals novel dynamics of pathway activation during primary and metastatic growth. Cancer Research, 64, 7336–7345.PubMedCrossRef
143.
Zurück zum Zitat Regot, S., Hughey, J. J., Bajar, B. T., Carrasco, S., & Covert, M. W. (2014). High-sensitivity measurements of multiple kinase activities in live single cells. Cell, 157, 1724–1734.PubMedPubMedCentralCrossRef Regot, S., Hughey, J. J., Bajar, B. T., Carrasco, S., & Covert, M. W. (2014). High-sensitivity measurements of multiple kinase activities in live single cells. Cell, 157, 1724–1734.PubMedPubMedCentralCrossRef
144.
Zurück zum Zitat Yano, S., Tazawa, H., Kagawa, S., Fujiwara, T., & Hoffman, R. M. (2020). FUCCI Real-time cell-cycle imaging as a guide for designing improved cancer therapy: A review of innovative strategies to target quiescent chemo-resistant cancer cells. Cancers (Basel), 12. Yano, S., Tazawa, H., Kagawa, S., Fujiwara, T., & Hoffman, R. M. (2020). FUCCI Real-time cell-cycle imaging as a guide for designing improved cancer therapy: A review of innovative strategies to target quiescent chemo-resistant cancer cells. Cancers (Basel), 12.
145.
Zurück zum Zitat Sakaue-Sawano, A., & Miyawaki, A. (2014). Visualizing spatiotemporal dynamics of multicellular cell-cycle progressions with fucci technology. Cold Spring Harbor Protocols, 2014. Sakaue-Sawano, A., & Miyawaki, A. (2014). Visualizing spatiotemporal dynamics of multicellular cell-cycle progressions with fucci technology. Cold Spring Harbor Protocols, 2014.
146.
Zurück zum Zitat Sakaue-Sawano, A., et al. (2008). Visualizing spatiotemporal dynamics of multicellular cell-cycle progression. Cell, 132, 487–498.PubMedCrossRef Sakaue-Sawano, A., et al. (2008). Visualizing spatiotemporal dynamics of multicellular cell-cycle progression. Cell, 132, 487–498.PubMedCrossRef
147.
Zurück zum Zitat Oki, T., et al. (2014). A novel cell-cycle-indicator, mVenus-p27K-, identifies quiescent cells and visualizes G0-G1 transition. Scientific Reports, 4, 4012.PubMedPubMedCentralCrossRef Oki, T., et al. (2014). A novel cell-cycle-indicator, mVenus-p27K-, identifies quiescent cells and visualizes G0-G1 transition. Scientific Reports, 4, 4012.PubMedPubMedCentralCrossRef
148.
Zurück zum Zitat Spencer, S. L., et al. (2013). XThe proliferation-quiescence decision is controlled by a bifurcation in CDK2 activity at mitotic exit. Cell, 155, 369–383.PubMedPubMedCentralCrossRef Spencer, S. L., et al. (2013). XThe proliferation-quiescence decision is controlled by a bifurcation in CDK2 activity at mitotic exit. Cell, 155, 369–383.PubMedPubMedCentralCrossRef
149.
Zurück zum Zitat Freter, R., et al. (2021). Establishment of a fluorescent reporter of RNA-polymerase II activity to identify dormant cells. Nature Communications, 12, 3318.PubMedPubMedCentralCrossRef Freter, R., et al. (2021). Establishment of a fluorescent reporter of RNA-polymerase II activity to identify dormant cells. Nature Communications, 12, 3318.PubMedPubMedCentralCrossRef
150.
Zurück zum Zitat Owen, K. L., et al. (2020). Prostate cancer cell-intrinsic interferon signaling regulates dormancy and metastatic outgrowth in bone. EMBO Reports, 21, e50162.PubMedPubMedCentralCrossRef Owen, K. L., et al. (2020). Prostate cancer cell-intrinsic interferon signaling regulates dormancy and metastatic outgrowth in bone. EMBO Reports, 21, e50162.PubMedPubMedCentralCrossRef
151.
Zurück zum Zitat Khoo, W. H., et al. (2019). A niche-dependent myeloid transcriptome signature defines dormant myeloma cells. Blood, 134, 30–43.PubMedCrossRef Khoo, W. H., et al. (2019). A niche-dependent myeloid transcriptome signature defines dormant myeloma cells. Blood, 134, 30–43.PubMedCrossRef
154.
Zurück zum Zitat Pranzini, E., Raugei, G., & Taddei, M. L. (2022). Metabolic features of tumor dormancy: Possible therapeutic strategies. Cancers (Basel), 14. Pranzini, E., Raugei, G., & Taddei, M. L. (2022). Metabolic features of tumor dormancy: Possible therapeutic strategies. Cancers (Basel), 14.
157.
Zurück zum Zitat Ma, R.-Y., Black, A., & Qian, B.-Z. (2022). Macrophage diversity in cancer revisited in the era of single-cell omics. Trends in Immunology, 43, 546–563.PubMedCrossRef Ma, R.-Y., Black, A., & Qian, B.-Z. (2022). Macrophage diversity in cancer revisited in the era of single-cell omics. Trends in Immunology, 43, 546–563.PubMedCrossRef
Metadaten
Titel
Regulation of dormancy during tumor dissemination: the role of the ECM
verfasst von
Ananya Mukherjee
Jose Javier Bravo-Cordero
Publikationsdatum
21.02.2023
Verlag
Springer US
Erschienen in
Cancer and Metastasis Reviews / Ausgabe 1/2023
Print ISSN: 0167-7659
Elektronische ISSN: 1573-7233
DOI
https://doi.org/10.1007/s10555-023-10094-2

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