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CLC number: R737.9

On-line Access: 2015-01-05

Received: 2014-06-25

Revision Accepted: 2014-09-30

Crosschecked: 2014-12-19

Cited: 6

Clicked: 6898

Citations:  Bibtex RefMan EndNote GB/T7714

 ORCID:

Chen-fang DONG

http://orcid.org/0000-0003-1123-6732

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Journal of Zhejiang University SCIENCE B 2015 Vol.16 No.1 P.10-17

http://doi.org/10.1631/jzus.B1400172


Epigenetic and metabolic regulation of breast cancer stem cells


Author(s):  Hui-xin Liu, Xiao-li Li, Chen-fang Dong

Affiliation(s):  Department of Pathology and Pathophysiology, School of Medicine, Zhejiang University, Hangzhou 310058, China

Corresponding email(s):   chenfangdong@zju.edu.cn

Key Words:  Cancer stem cells (CSCs), Epithelial mesenchymal transition (EMT), Epigenetic modification, Metabolic reprogramming, Breast cancer


Hui-xin Liu, Xiao-li Li, Chen-fang Dong. Epigenetic and metabolic regulation of breast cancer stem cells[J]. Journal of Zhejiang University Science B, 2015, 16(1): 10-17.

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}

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DOI - 10.1631/jzus.B1400172


Abstract: 
breast cancer has a relatively high mortality rate in women due to recurrence and metastasis. Increasing evidence has identified a rare population of cells with stem cell-like properties in breast cancer. These cells, termed cancer stem cells (CSCs), which have the capacity for self-renewal and differentiation, contribute significantly to tumor progression, recurrence, drug resistance and metastasis. Clarifying the mechanisms regulating breast CSCs has important implications for our understanding of breast cancer progression and therapeutics. A strong connection has been found between breast CSCs and epithelial mesenchymal transition (EMT). In addition, recent studies suggest that the maintenance of the breast CSC phenotype is associated with epigenetic and metabolic regulation. In this review, we focus on recent discoveries about the connection between EMT and CSC, and advances made in understanding the roles and mechanisms of epigenetic and metabolic reprogramming in controlling breast CSC properties.

This is a concise and well written review. The authors have reviewed the most recent developments in the field of breast cancer and their own work.

表观遗传修饰和代谢重编程对乳腺癌干细胞的调控

概要:乳腺癌已居我国女性恶性肿瘤死亡率首位。近来研究表明,乳腺肿瘤组织内有少量具有自我更新和分化潜能的肿瘤干细胞,这些肿瘤干细胞在乳腺癌发生、发展、转移及复发过程中起关键作用。深入研究乳腺癌干细胞的调控机制对乳腺癌的预防和治疗具有十分重要意义。本文综合近期的研究成果,概括了表观遗传修饰和代谢重编程对上皮间质转化及乳腺癌干细胞的调控机制,且系统地分析与总结了表观遗传修饰、代谢重编程、上皮间质转化和乳腺癌干细胞之间的相互关系。

关键词:肿瘤干细胞;上皮间质转化;表观遗传修饰;代谢重编程;乳腺癌

Darkslateblue:Affiliate; Royal Blue:Author; Turquoise:Article

Reference

[1]Al-Hajj, M., Wicha, M.S., Benito-Hernandez, A., et al., 2003. Prospective identification of tumorigenic breast cancer cells. PNAS, 100(7):3983-3988.

[2]Allegrucci, C., Wu, Y.Z., Thurston, A., et al., 2007. Restriction landmark genome scanning identifies culture-induced DNA methylation instability in the human embryonic stem cell epigenome. Hum. Mol. Genet., 16(10):1253-1268.

[3]Almendro, V., Fuster, G., 2011. Heterogeneity of breast cancer: etiology and clinical relevance. Clin. Transl. Oncol., 13(11):767-773.

[4]Armstrong, L., Tilgner, K., Saretzki, G., et al., 2010. Human induced pluripotent stem cell lines show stress defense mechanisms and mitochondrial regulation similar to those of human embryonic stem cells. Stem Cells, 28(4):661-673.

[5]Barski, A., Cuddapah, S., Cui, K., et al., 2007. High-resolution profiling of histone methylations in the human genome. Cell, 129(4):823-837.

[6]Blick, T., Hugo, H., Widodo, E., et al., 2010. Epithelial mesenchymal transition traits in human breast cancer cell lines parallel the CD44hi/CD24lo/− stem cell phenotype in human breast cancer. J. Mammary Gland Biol. Neoplasia, 15(2):235-252.

[7]Bloushtain-Qimron, N., Yao, J., Snyder, E.L., et al., 2008. Cell type-specific DNA methylation patterns in the human breast. PNAS, 105(37):14076-14081.

[8]Bowerman, B., 2005. Cell biology. Oxidative stress and cancer: a β-catenin convergence. Science, 308(5725):1119-1120.

[9]Bracken, A.P., Dietrich, N., Pasini, D., et al., 2006. Genome-wide mapping of Polycomb target genes unravels their roles in cell fate transitions. Genes Dev., 20(9):1123-1136.

[10]Campos, E.I., Reinberg, D., 2009. Histones: annotating chromatin. Annu. Rev. Genet., 43(1):559-599.

[11]Cedar, H., Bergman, Y., 2009. Linking DNA methylation and histone modification: patterns and paradigms. Nat. Rev. Genet., 10(5):295-304.

[12]Clevers, H., 2006. Wnt/β-catenin signaling in development and disease. Cell, 127(3):469-480.

[13]Diehn, M., Cho, R.W., Lobo, N.A., et al., 2009. Association of reactive oxygen species levels and radioresistance in cancer stem cells. Nature, 458(7239):780-783.

[14]Dong, C., Wu, Y., Yao, J., et al., 2012. G9a interacts with Snail and is critical for Snail-mediated E-cadherin repression in human breast cancer. J. Clin. Invest., 122(4):1469-1486.

[15]Dong, C., Wu, Y., Yao, J., et al., 2013a. Interaction with Suv39H1 is critical for Snail-mediated E-cadherin repression in breast cancer. Oncogene, 32(11):1351-1362.

[16]Dong, C., Yuan, T., Wu, Y., et al., 2013b. Loss of FBP1 by Snail-mediated repression provides metabolic advantages in basal-like breast cancer. Cancer Cell, 23(3):316-331.

[17]Dontu, G., Abdallah, W.M., Foley, J.M., et al., 2003. In vitro propagation and transcriptional profiling of human mammary stem/progenitor cells. Genes Dev., 17(10):1253-1270.

[18]Driessens, G., Beck, B., Caauwe, A., et al., 2012. Defining the mode of tumour growth by clonal analysis. Nature, 488(7412):527-530.

[19]Essers, M.A., de Vries-Smits, L.M., Barker, N., et al., 2005. Functional interaction between β-catenin and FOXO in oxidative stress signaling. Science, 308(5725):1181-1184.

[20]Facucho-Oliveira, J.M., St. John, J.C., 2009. The relationship between pluripotency and mitochondrial DNA proliferation during early embryo development and embryonic stem cell differentiation. Stem Cell Rev. Rep., 5(2):140-158.

[21]Fillmore, C., Kuperwasser, C., 2007. Human breast cancer stem cell markers CD44 and CD24: enriching for cells with functional properties in mice or in man. Breast Cancer Res., 9(3):303.

[22]Folmes, C.D., Nelson, T.J., Martinez-Fernandez, A., et al., 2011. Somatic oxidative bioenergetics transitions into pluripotency-dependent glycolysis to facilitate nuclear reprogramming. Cell Metab., 14(2):264-271.

[23]Gerhard, R., Ricardo, S., Albergaria, A., et al., 2012. Immunohistochemical features of claudin-low intrinsic subtype in metaplastic breast carcinomas. Breast, 21(3):354-360.

[24]Ginestier, C., Hur, M.H., Charafe-Jauffret, E., et al., 2007. ALDH1 is a marker of normal and malignant human mammary stem cells and a predictor of poor clinical outcome. Cell Stem Cell, 1(5):555-567.

[25]Greene, S.B., Herschkowitz, J.I., Rosen, J.M., 2010. Small players with big roles: microRNAs as targets to inhibit breast cancer progression. Curr. Drug Targets, 11(9):1059-1073.

[26]Grewal, S.I., Jia, S., 2007. Heterochromatin revisited. Nat. Rev. Genet., 8(1):35-46.

[27]Gupta, P.B., Fillmore, C.M., Jiang, G., et al., 2011. Stochastic state transitions give rise to phenotypic equilibrium in populations of cancer cells. Cell, 146(4):633-644.

[28]Hennessy, B.T., Gonzalez-Angulo, A.M., Stemke-Hale, K., et al., 2009. Characterization of a naturally occurring breast cancer subset enriched in epithelial-to-mesenchymal transition and stem cell characteristics. Cancer Res., 69(10):4116-4124.

[29]Holm, K., Grabau, D., Lovgren, K., et al., 2012. Global H3K27 trimethylation and EZH2 abundance in breast tumor subtypes. Mol. Oncol., 6(5):494-506.

[30]Jemal, A., Bray, F., Center, M.M., et al., 2011. Global cancer statistics. CA Cancer J. Clin., 61(2):69-90.

[31]Jordan, C.T., Guzman, M.L., Noble, M., 2006. Cancer stem cells. N. Engl. J. Med., 355(12):1253-1261.

[32]Keller, P.J., Arendt, L.M., Skibinski, A., et al., 2012. Defining the cellular precursors to human breast cancer. PNAS, 109(8):2772-2777.

[33]Lee, T.I., Jenner, R.G., Boyer, L.A., et al., 2006. Control of developmental regulators by Polycomb in human embryonic stem cells. Cell, 125(2):301-313.

[34]Lin, Y., Wu, Y., Li, J., et al., 2010. The SNAG domain of Snail1 functions as a molecular hook for recruiting lysine-specific demethylase 1. EMBO J., 29(11):1803-1816.

[35]Mallick, B., Chakrabarti, J., Ghosh, Z., 2011. MicroRNA reins in embryonic and cancer stem cells. RNA Biol., 8(3):415-426.

[36]Mani, S.A., Guo, W., Liao, M.J., et al., 2008. The epithelial-mesenchymal transition generates cells with properties of stem cells. Cell, 133(4):704-715.

[37]McCabe, M.T., Brandes, J.C., Vertino, P.M., 2009. Cancer DNA methylation: molecular mechanisms and clinical implications. Clin. Cancer Res., 15(12):3927-3937.

[38]Meyer, M.J., Fleming, J.M., Ali, M.A., et al., 2009. Dynamic regulation of CD24 and the invasive, CD44posCD24neg phenotype in breast cancer cell lines. Breast Cancer Res., 11(6):R82.

[39]Mohn, F., Schubeler, D., 2009. Genetics and epigenetics: stability and plasticity during cellular differentiation. Trends Genet., 25(3):129-136.

[40]Morel, A.P., Lievre, M., Thomas, C., et al., 2008. Generation of breast cancer stem cells through epithelial-mesenchymal transition. PLoS ONE, 3(8):e2888.

[41]Nieto, M.A., 2011. The ins and outs of the epithelial to mesenchymal transition in health and disease. Annu. Rev. Cell Dev. Biol., 27(1):347-376.

[42]Pasini, D., Bracken, A.P., Hansen, J.B., et al., 2007. The polycomb group protein Suz12 is required for embryonic stem cell differentiation. Mol. Cell. Biol., 27(10):3769-3779.

[43]Perou, C.M., Sorlie, T., Eisen, M.B., et al., 2000. Molecular portraits of human breast tumours. Nature, 406(6797):747-752.

[44]Polyak, K., 2011. Heterogeneity in breast cancer. J. Clin. Invest., 121(10):3786-3788.

[45]Polyak, K., Weinberg, R.A., 2009. Transitions between epithelial and mesenchymal states: acquisition of malignant and stem cell traits. Nat. Rev. Cancer, 9(4):265-273.

[46]Prigione, A., Fauler, B., Lurz, R., et al., 2010. The senescence-related mitochondrial/oxidative stress pathway is repressed in human induced pluripotent stem cells. Stem Cells, 28(4):721-733.

[47]Proia, T.A., Keller, P.J., Gupta, P.B., et al., 2011. Genetic predisposition directs breast cancer phenotype by dictating progenitor cell fate. Cell Stem Cell, 8(2):149-163.

[48]Reik, W., 2007. Stability and flexibility of epigenetic gene regulation in mammalian development. Nature, 447(7143):425-432.

[49]Sarrio, D., Rodriguez-Pinilla, S.M., Hardisson, D., et al., 2008. Epithelial-mesenchymal transition in breast cancer relates to the basal-like phenotype. Cancer Res., 68(4):989-997.

[50]Shah, M., Allegrucci, C., 2012. Keeping an open mind: highlights and controversies of the breast cancer stem cell theory. Breast Cancer (Dove Med. Press), 4:155-166.

[51]Shi, Y., 2007. Histone lysine demethylases: emerging roles in development, physiology and disease. Nat. Rev. Genet., 8(11):829-833.

[52]Shimono, Y., Zabala, M., Cho, R.W., et al., 2009. Downregulation of miRNA-200c links breast cancer stem cells with normal stem cells. Cell, 138(3):592-603.

[53]Thiery, J.P., Acloque, H., Huang, R.Y., et al., 2009. Epithelial-mesenchymal transitions in development and disease. Cell, 139(5):871-890.

[54]Tothova, Z., Kollipara, R., Huntly, B.J., et al., 2007. FoxOs are critical mediators of hematopoietic stem cell resistance to physiologic oxidative stress. Cell, 128(2):325-339.

[55]Wellner, U., Schubert, J., Burk, U.C., et al., 2009. The EMT-activator ZEB1 promotes tumorigenicity by repressing stemness-inhibiting microRNAs. Nat. Cell Biol., 11(12):1487-1495.

[56]Wicha, M.S., Liu, S., Dontu, G., 2006. Cancer stem cells: an old idea—a paradigm shift. Cancer Res., 66(4):1883-1890; discussion 1895-1896.

[57]Yu, F., Yao, H., Zhu, P., et al., 2007. let-7 regulates self renewal and tumorigenicity of breast cancer cells. Cell, 131(6):1109-1123.

[58]Zhu, S., Li, W., Zhou, H., et al., 2010. Reprogramming of human primary somatic cells by OCT4 and chemical compounds. Cell Stem Cell, 7(6):651-655.

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