Cellullar Plasticity and Dedifferentiation: A Link Between Cancer Stem Cells, Hypoxia, Cell Injury, and Inflammation
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Cellular plasticity is the concept of bidirectional dynamics change cells differentiation degree which involved in the regeneration, repair and tissue turnover along the organism livespan. Cellular plasticity and dedifferentiation process are well documented in the discovery of iPCSs by introducing several transcriptional factors known as Yamanaka factor to terminally differentiated somatic cells and reverted into pluripotent state as the ESCs. iPSCs are able to exhibit ESCs differentiation potential which could produce ectodermic, mesodermic, and endodermic cell lineage. In tumour biology, the tumour plasticity also have a similar regulation and play an imporant role for maintaining tumour integrity and survival, particularly in maintaining CSCs population. Various study of cellular plasticity regulation has shown that various factors are involved, in example hypoxia, cell injury, and inflammation. Cells respond to hypoxia, cell injury, and inflammation by chemoattractant which attract repair cells to homing towards injured sites. The homing mechanism of stem cells involved EMT to facilitates migration of stem cells towards injured sites, thus leading to tissue regeneration. On the other hand, cancer metastasis also showed a connection with EMT process. EMT which showed a change in cell properties are linked to dedifferentiation and hypoxia response. Hypoxia condition has been known to preserve and both normal stem cells and CSCs stemness. HIF which protected from degradation in hypoxia condition interact with DNA by binding to HRE. HRE activation trigger transcription of numerous signalling protein which involved in stemness, cell proliferation and survival. Therefore it is concluded that cell injury, hypoxia, and inflammation could programmed cells to undergo dedifferentiation process and involved in EMT regulations. CSCs which resides insides heterogeneous tumour cells population are though to be dynamicly regulate itself in the quietscent and active state through dedifferentiation like the normal stem cells. Understanding how CSCs regulates its active an quietscent state dynamics could provide an important information for novel CSCs targeted therapy development.
Abdollahi, H., Harris, L.J., Zhang, P., McIlhenny, S., Srinivas, V., Tulenko, T., DiMuzio, P.J., 2011. The Role of Hypoxia in Stem Cell Differentiation and Therapeutics. J. Surg. Res. 165, 112–117.
Abdullah, L.N., Chow, E.K.-H., 2013. Mechanisms of chemoresistance in cancer stem cells. Clin. Transl. Med. 2, 3.
Ahmed, N.E.M.B., Murakami, M., Kaneko, S., Nakashima, M., 2016. The effects of hypoxia on the stemness properties of human dental pulp stem cells (DPSCs). Sci. Rep. 6, 1–10.
Al-Hajj, M., Wicha, M.S., Benito-Hernandez, A., Morrison, S.J., Clarke, M.F., 2003. Prospective identification of tumorigenic breast cancer cells. Proc. Natl. Acad. Sci. U. S. A. 100, 3983–3988.
Alvarez, C. V., Garcia-Lavandeira, M., Garcia-Rendueles, M.E.R., Diaz-Rodriguez, E., Garcia-Rendueles, A.R., Perez-Romero, S., Vila, T.V., Rodrigues, J.S., Lear, P. V., Bravo, S.B., 2012. Defining stem cell types: Understanding the therapeutic potential of ESCs, ASCs, and iPS cells. J. Mol. Endocrinol. 49.
Anders, H.-J., Schaefer, L., 2014. Beyond Tissue Injury”Damage-Associated Molecular Patterns, Toll-Like Receptors, and Inflammasomes Also Drive Regeneration and Fibrosis. J Am Soc Nephrol Jul 25.
Aurora, A.B., Olson, E.N., 2015. Immune Modulation of Stem Cells and Regeneration. Cell Stem Cell. 15, 14–25.
Baraniak, P.R., McDevitt, T.C., 2010. Stem cell paracrine actions and tissue regeneration. Regen. Med. 5, 121–143.
Blanpain, C., Mohrin, M., Sotiropoulou, P.A., Passegué, E., 2011. DNA-Damage Response in Tissue-Specific and Cancer Stem Cells. Cell Stem Cell 8, 16–29.
Bodnar, R.J., 2013. Epidermal Growth Factor and Epidermal Growth Factor Receptor: The Yin and Yang in the Treatment of Cutaneous Wounds and Cancer. Adv. wound care 2, 24–29.
Bomken, S., FiÅ¡er, K., Heidenreich, O., Vormoor, J., 2010. Understanding the cancer stem cell. Br. J. Cancer 103, 439–445.
Bonnet, D., Dick, J.E., 1997. Human acute myeloid leukemia is organized as a hierarchy that originates from a primitive hematopoietic cell. Nat. Med. 3, 730–737.
Borovski, T., De Sousa E Melo, F., Vermeulen, L., Medema, J.P., 2011. Cancer stem cell niche: The place to be. Cancer Res. 71, 634–639.
Bray, F., Ferlay, J., Soerjomataram, I., Siegel, R., Torre, L., Jemal, A., 2018. Global cancer statistics 2018: GLOBOCAN estimates of incidence and mortality worldwide for 36 cancers in 185 countries. CA A J. Clin. 00, 1–31.
Calvani, M., Rapisarda, A., Uranchimeg, B., Shoemaker, R.H., Melillo, G., 2006. Hypoxic induction of an HIF-1alpha-dependent bFGF autocrine loop drives angiogenesis in human endothelial cells. Blood 107, 2705–2712.
Campos, B., Wan, F., Farhadi, M., Ernst, A., Zeppernick, F., Tagscherer, K.E., Ahmadi, R., Lohr, J., Dictus, C., Gdynia, G., Combs, S.E., Goidts, V., Helmke, B.M., Eckstein, V., Roth, W., Beckhove, P., Lichter, P., Unterberg, A., Radlwimmer, B., Herold-Mende, C., 2010. Differentiation Therapy Exerts Antitumor Effects on Stem-like Glioma Cells. Clin. Cancer Res. 16, 2715–2728.
Carlson, M.E., Conboy, I.M., 2007. Loss of stem cell regenerative capacity within aged niches. Aging Cell 6, 371–382.
Cavaillon, J.M., 2001. Pro- versus anti-inflammatory cytokines: myth or reality. Cell. Mol. Biol. (Noisy-le-grand). 47, 695–702.
de-Leon, S.B.-T., Davidson, E.H., 2007. Gene Regulation: Gene Control Network in Development. Annu. Rev. Biophys. Biomol. Struct. 36, 191–212.
De Thé, H., 2018. Differentiation therapy revisited. Nat. Rev. Cancer 18, 117–127.
Discher, D.E., Mooney, D.J., Zandstra, P.W., 2010. Growth factors, matrices, and forces combine and control stem cells. Science (80-. ). 324, 1673–1677.
Falanga, V., 2012. Stem Cells in Tissue Repair and Regeneration. J. Invest. Dermatol. 132, 1538–1541.
Fillmore, C.M., Kuperwasser, C., 2008. Human breast cancer cell lines contain stem-like cells that self-renew, give rise to phenotypically diverse progeny and survive chemotherapy. Breast Cancer Res 10.
Fong, E.L.S., Chan, C.K., Goodman, S.B., 2011. Stem cell homing in musculoskeletal injury. Biomaterials 32, 395–409.
Francis, K.R., Wei, L., 2010. Human embryonic stem cell neural differentiation and enhanced cell survival promoted by hypoxic preconditioning. Cell Death Dis. 1, e22-11.
Gnecchi, M., Zhang, Z., Ni, A., Dzau, V.J., 2008. Paracrine mechanisms in adult stem cell signaling and therapy. Circ. Res. 103, 1204–1219.
Gómez-López, S., Lerner, R.G., Petritsch, C., 2014. Asymmetric cell division of stem and progenitor cells during homeostasis and cancer. Cell. Mol. Life Sci. 71, 575–597.
Gurtner, G.C., Werner, S., Barrandon, Y., Longaker, M.T., 2008. Wound repair and regeneration. Nature 453, 314–321.
Halme, D.G., Kessler, D.A., 2006. FDA Regulation of Stem-Cell–Based Therapies. N. Engl. J. Med. 355, 1730–1735.
Han, Z.B., Ren, H., Zhao, H., Chi, Y., Chen, K., Zhou, B., Liu, Y.J., Zhang, L., Xu, B., Liu, B., Yang, R., Han, Z.C., 2008. Hypoxia-inducible factor (HIF)-1α directly enhances the transcriptional activity of stem cell factor (SCF) in response to hypoxia and epidermal growth factor (EGF). Carcinogenesis 29, 1853–1861.
Hayflick, L., Moorhead, P.S., 1961. The serial cultivation of human diploid cell strains. Exp. Cell Res. 25, 585–621.
Heddleston, J.M., Li, Z., Lathia, J.D., Bao, S., Hjelmeland, A.B., Rich, J.N., 2010. Hypoxia inducible factors in cancer stem cells. Br J Cancer 102.
Hocking, A.M., Gibran, N.S., 2010. Mesenchymal stem cells: paracrine signaling and differentiation during cutaneous wound repair. Exp. Cell Res. 316, 2213–2219.
Ignazio, L.D., Batie, M., Rocha, S., 2017. Hypoxia and Inflammation in Cancer, Focus on HIF and NF-κB. Biomedicines 5, 21.
Ignazio, L.D., Rocha, S., 2016. Hypoxia Induced NF- κ B 1–8.
Jaenisch, R., Young, R., 2008. Stem Cells, the Molecular Circuitry of Pluripotency and Nuclear Reprogramming. Cell 132, 567–582.
Jögi, A., í˜ra, I., Nilsson, H., Poellinger, L., Axelson, H., Påhlman, S., 2003. Hypoxia-induced dedifferentiation in neuroblastoma cells. Cancer Lett. 197, 145–150.
Khavari, D.A., Sen, G.L., Rinn, J.L., 2010. DNA methylation and epigenetic control of cellular differentiation. Cell Cycle 9, 3880–3883.
Khong, T.L., Thairu, N., Larsen, H., Dawson, P.M., Kiriakidis, S., Paleolog, E.M., 2013. Identification of the angiogenic gene signature induced by EGF and hypoxia in colorectal cancer. BMC Cancer 13, 518.
Kragl, M., Knapp, D., Nacu, E., Khattak, S., Maden, M., Epperlein, H.H., Tanaka, E.M., 2009. Cells keep a memory of their tissue origin during axolotl limb regeneration. Nature 460, 60–65.
Laitala, A., Erler, J.T., 2018. Hypoxic Signalling in Tumour Stroma. Front. Oncol. 8, 1–13.
Lennartsson, J., Ronnstrand, L., 2012. Stem Cell Factor Receptor/c-Kit: From Basic Science to Clinical Implications. Physiol. Rev. 92, 1619–1649.
Li, L., Clevers, H., 2010. Coexistence of Quiescent and Active Adult Stem Cells in Mammals. Science (80-. ). 327, 542–545.
Li, Q., Xue, X., Li, W., Wang, Q., Han, L., Brunson, T., Xu, W., Chambers-Harris, I., Wang, Q., Li, X., Ma, L., Song, Q., 2017. Heterogeneous DNA methylation status in same-cell subpopulations of ovarian cancer tissues. Tumor Biol. 39, 0–7.
Li, Y., Rogoff, H. a, Keates, S., Gao, Y., Murikipudi, S., Mikule, K., Leggett, D., Li, W., Pardee, A.B., Li, C.J., 2015. Suppression of cancer relapse and metastasis by inhibiting cancer stemness. Proc. Natl. Acad. Sci. U. S. A. 112, 1839–1844.
Liu, Y., Singh, S.R., Zeng, X., Zhao, J., Hou, S.X., 2016. The Nuclear Matrix Protein Megator Regulates Stem Cell Asymmetric Division through the Mitotic Checkpoint Complex in Drosophila Testes. PLOS Genet. 11, e1005750.
Magee, J.A., Piskounova, E., Morrison, S.J., 2012. Cancer Stem Cells: Impact, Heterogeneity, and Uncertainty. Cancer Cell 21, 283–296.
Maric, D., Maric, I., Chang, Y.H., Barker, J.L., 2003. Prospective cell sorting of embryonic rat neural stem cells and neuronal and glial progenitors reveals selective effects of basic fibroblast growth factor and epidermal growth factor on self-renewal and differentiation. J.Neurosci. 23, 240–251.
Mason, C., Dunnill, P., 2008a. A brief definition of regenerative medicine. Regen. Med. 3, 1–5.
Mason, C., Dunnill, P., 2008b. A brief definition of regenerative medicine. Regen. Med. 3, 1–5.
Maugeri-Saccí , M., Bartucci, M., De Maria, R., 2012. DNA damage repair pathways in cancer stem cells. Mol. Cancer Ther. 11, 1627–36.
Moitra, K., 2015. Overcoming Multidrug Resistance in Cancer Stem Cells. Biomed Res. Int. 2015, 1–8.
Muz, B., de la Puente, P., Azab, F., Luderer, M., Azab, A.K., 2014. Hypoxia promotes stem cell-like phenotype in multiple myeloma cells. Blood Cancer J. 4, e262.
Newton, K., Dixit, V.M., 2012. Signaling in Innate Immunity and Inflammation. Cold Spring Harb. Perspect. Biol. 4, a006049–a006049.
Nishi, H., Nakada, T., Kyo, S., Inoue, M., Shay, J.W., Isaka, K., 2004. Hypoxia-Inducible Factor 1 Mediates Upregulation of Telomerase (hTERT). Mol. Cell. Biol. 24, 6076–6083.
Nordmann, T.M., Dror, E., Schulze, F., Traub, S., Berishvili, E., Barbieux, C., Böni-Schnetzler, M., Donath, M.Y., 2017. The Role of Inflammation in β-cell Dedifferentiation. Sci. Rep. 7, 1–10.
Poss, K.D., 2010. Advances in understanding tissue regenerative capacity and mechanisms in animals. Nat. Rev. Genet. 11, 710–722.
Rantam, F.A., Ferdiansyah, Purwati, 2014. Stem Cell Mesenchimal, Hematopoetik, dan Model Aplikasi, 2nd ed. Airlangga University Press, Surabaya.
Raveh-Amit, H., Berzsenyi, S., Vas, V., Ye, D., Dinnyes, A., 2013. Tissue resident stem cells: till death do us part. Biogerontology 14, 573–590.
Riehle, K.J., Dan, Y.Y., Campbell, J.S., Fausto, N., 2011. New concepts in liver regeneration. J. Gastroenterol. Hepatol. 26 Suppl 1, 203–212.
Sánchez Alvarado, A., 2012. Q&A: What is regeneration, and why look to planarians for answers? BMC Biol. 10, 88.
Satyanarayana, A., Wiemann, S.U., Buer, J., Lauber, J., Dittmar, K.E.J., Wüstefeld, T., Blasco, M.A., Manns, M.P., Rudolph, K.L., 2003. Telomere shortening impairs organ regeneration by inhibiting cell cycle re-entry of a subpopulation of cells. EMBO J. 22, 4003–4013.
Seyfried, T.N., 2012. Cancer as a Metabolic Disease. John Wiley & Sons, Inc., New Jersey.
Shay, J.W., Wright, W.E., 2000. Hayflick, his limit, and cellular ageing. Nat. Rev. Mol. Cell Biol. 1, 72.
Shi, Y.H., Wang, Y.X., Bingle, L., Gong, L.H., Heng, W.J., Li, Y., Fang, W.G., 2005. In vitro study of HIF-1 activation and VEGF release by bFGF in the T47D breast cancer cell line under normoxic conditions: Involvement of PI-3K/Akt and MEK1/ERK pathways. J. Pathol. 205, 530–536.
Shook, B., Rivera Gonzalez, G., Ebmeier, S., Grisotti, G., Zwick, R., Horsley, V., 2016. The Role of Adipocytes in Tissue Regeneration and Stem Cell Niches. Annu. Rev. Cell Dev. Biol. 32, 609–631.
Sporn, M.B., Roberts, A.B., 1986. Peptide growth factors and inflammation, tissue repair, and cancer. J. Clin. Invest. 78, 329–332.
Srivastava, A.K., Bulte, J.W.M., 2014. Seeing stem cells at work in vivo. Stem Cell Rev. 10, 127–144.
Takahashi, K., Yamanaka, S., 2006. Induction of pluripotent stem cells from mouse embryonic and adult fibroblast cultures by defined factors. Cell 126, 663–76.
Tao, R., Sun, T.J., Han, Y.Q., Xu, G., Liu, J., Han, Y.F., 2014. Optimization of in vitro cell labeling methods for human umbilical cord-derived mesenchymal stem cells. Eur. Rev. Med. Pharmacol. Sci. 18, 1127–1134.
Tetteh, P.W., Farin, H.F., Clevers, H., 2015. Plasticity within stem cell hierarchies in mammalian epithelia. Trends Cell Biol. 25, 100–108.
Tsai, C.C., Chen, Y.J., Yew, T.L., Chen, L.L., Wang, J.Y., Chiu, C.H., Hung, S.C., 2011. Hypoxia inhibits senescence and maintains mesenchymal stem cell properties through down-regulation of E2A-p21 by HIF-TWIST. Blood 117, 459–469.
Ullah, M., Sun, Z., 2018. Stem cells and anti-aging genes: double-edged sword-do the same job of life extension. Stem Cell Res. Ther. 9, 3.
Vermeulen, L., De Sousa E Melo, F., van der Heijden, M., Cameron, K., de Jong, J.H., Borovski, T., Tuynman, J.B., Todaro, M., Merz, C., Rodermond, H., Sprick, M.R., Kemper, K., Richel, D.J., Stassi, G., Medema, J.P., 2010. Wnt activity defines colon cancer stem cells and is regulated by the microenvironment. Nat. Cell Biol. 12, 468.
Von Figura, G., Hartmann, D., Song, Z., Rudolph, K.L., 2009. Role of telomere dysfunction in aging and its detection by biomarkers. J. Mol. Med. 87, 1165–1171.
Walter, J.B., Talbot, I.C., Gardner, H.A., et. al., 1996. General Pathology, 7th ed. Churchill Livingstone, New York.
Wang, P., Wan, W., Xiong, S.-L., Feng, H., Wu, N., 2017a. Cancer stem-like cells can be induced through dedifferentiation under hypoxic conditions in glioma, hepatoma and lung cancer. Cell Death Discov. 3, 16105.
Wang, P., Wan, W., Xiong, S., Wang, J., Zou, D., Lan, C., Yu, S., Liao, B., Feng, H., Wu, N., 2017b. HIF1α regulates glioma chemosensitivity through the transformation between differentiation and dedifferentiation in various oxygen levels. Sci. Rep. 7, 1–16.
Wang, R., Lv, Q., Meng, W., Tan, Q., Zhang, S., Mo, X., Yang, X., 2014. Comparison of mammosphere formation from breast cancer cell lines and primary breast tumors. J. Thorac. Dis. 6, 829–837.
Wang, Y., Roche, O., Xu, C., Moriyama, E.H., Heir, P., Chung, J., Roos, F.C., Chen, Y., Finak, G., Milosevic, M., Wilson, B.C., Teh, B.T., Park, M., Irwin, M.S., Ohh, M., 2012. Hypoxia promotes ligand-independent EGF receptor signaling via hypoxia-inducible factor{textendash}mediated upregulation of caveolin-1. Proc. Natl. Acad. Sci. 109, 4892–4897.
Wen, W., Zhang, M., 2018. Protein Complex Assemblies in Epithelial Cell Polarity and Asymmetric Cell Division. J. Mol. Biol. 430, 3504–3520.
Wiemann, S.U., Satyanarayana, A., Tsahuridu, M., Tillmann, H.L., Zender, L., Klempnauer, J., Flemming, P., Franco, S., Blasco, M.A., MANNS, M.P., RUDOLPH, K.L., 2002. Hepatocyte telomere shortening and senescence are general markers of human liver cirrhosis. FASEB J. 16, 935–942.
Xu, H., Yu, S., Liu, Q., Yuan, X., Mani, S., Pestell, R.G., Wu, K., 2017. Recent advances of highly selective CDK4/6 inhibitors in breast cancer. J. Hematol. Oncol. 10, 97.
Yamanaka, S., 2010. Patient-Specific Pluripotent Stem Cells Become Even More Accessible. Cell Stem Cell 7, 1–2.
Yatabe, N., Kyo, S., Maida, Y., Nishi, H., Nakamura, M., Kanaya, T., Tanaka, M., Isaka, K., Ogawa, S., Inoue, M., 2004. HIF-1-mediated activation of telomerase in cervical cancer cells. Oncogene 23, 3708–3715.
Zhang, Y., 2009. Autologous cell sources for urological applications. In: Drenstedt, J., Atala, A. (Eds.), Biomaterials and Tissue Engineering in Urology. CRC Press, Cambridge, pp. 334–356.
Zhou, Y., Fan, W., Xiao, Y., 2014. The effect of hypoxia on the stemness and differentiation capacity of PDLC and DPC. Biomed Res. Int. 2014.
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