17β-estradiol regulates the malignancy of cancer stem-like cells derived from the MCF7 cell line partially through Sox2

Guo,Lian; Li,Feng; Wang,Mengyuan; Xu,Yue; Wang,Bangqiong; Ran,Dongchuan; Zhang,Xianxiang

doi:10.3892/ol.2018.7796

17β-estradiol regulates the malignancy of cancer stem-like cells derived from the MCF7 cell line partially through Sox2

Authors:
- Lian Guo
- Feng Li
- Mengyuan Wang
- Yue Xu
- Bangqiong Wang
- Dongchuan Ran
- Xianxiang Zhang
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Affiliations: Department of Endocrinology, Chongqing Three Gorges Central Hospital, Wanzhou, Chongqing 404000, P.R. China
Published online on: January 15, 2018 https://doi.org/10.3892/ol.2018.7796
Pages: 3790-3795

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Abstract

As a major common malignant tumor in women, the malignant behavior of breast cancer, which includes tumorigenesis and metastasis, is associated with estrogen, particularly 17β-estradiol (E2). With accumulating evidence demonstrating that cancer stem-like cells (CSCs) serve a function in the malignant behavior of breast cancer, including metastasis, recurrence and chemoresistance, the effects of E2 on the physiological processes of CSCs have been attracting more attention. In the present study, in order to investigate the effects of E2 on CSCs, CSCs from the MCF7 breast cancer cell line were isolated and treated with 1, 10 and 50 nM E2. Detection of cell proliferation following E2 treatment revealed that 10 nM E2 treatment inhibited cell proliferation, whereas 50 nM E2 treatment resulted in the induction of apoptosis on CSCs. In order to further investigate the effects of E2 treatment on migration, colony formation and the self-renewal capacity of CSCs in vitro, cells were treated with 1 and 10 nM E2. As expected, compared with mock group, the self-renewal capacity of the CSCs was slightly increased by 10 nM E2 treatment, while 1 nM exhibited no observable effect. E2 treatment demonstrated different effects on the proliferation, migration, colony formation and self-renewal capacity of CSCs in a dose-dependent manner.

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1	Siegel R, Naishadham D and Jemal A: Cancer statistics, 2013. CA Cancer J Clin. 63:11–30. 2013. View Article : Google Scholar : PubMed/NCBI
2	Landis MD, Lehmann BD, Pietenpol JA and Chang JC: Patient-derived breast tumor xenografts facilitating personalized cancer therapy. Breast Cancer Res. 15:2012013. View Article : Google Scholar : PubMed/NCBI
3	Hulka BS and Moorman PG: Breast cancer: Hormones and other risk factors. Maturitas. 38:103–116. 2001. View Article : Google Scholar : PubMed/NCBI
4	Moore NM and Nagahara LA: Physical biology in cancer. 1. Cellular physics of cancer metastasis. Am J Physiol Cell Physiol. 306:C78–C79. 2014. View Article : Google Scholar : PubMed/NCBI
5	Osborne CK and Schiff R: Estrogen-receptor biology: Continuing progress and therapeutic implications. J Clin Oncol. 23:1616–1622. 2005. View Article : Google Scholar : PubMed/NCBI
6	Doisneau-Sixou SF, Sergio CM, Carroll JS, Hui R, Musgrove EA and Sutherland RL: Estrogen and antiestrogen regulation of cell cycle progression in breast cancer cells. Endocr Relat Cancer. 10:179–186. 2003. View Article : Google Scholar : PubMed/NCBI
7	Cunliffe HE, Ringnér M, Bilke S, Walker RL, Cheung JM, Chen Y and Meltzer PS: The gene expression response of breast cancer to growth regulators: Patterns and correlation with tumor expression profiles. Cancer Res. 63:7158–7166. 2003.PubMed/NCBI
8	Basu A and Rowan BG: Genes related to estrogen action in reproduction and breast cancer. Front Biosci. 10:2346–2372. 2005. View Article : Google Scholar : PubMed/NCBI
9	Deroo BJ and Korach KS: Estrogen receptors and human disease. J Clin Invest. 116:561–570. 2006. View Article : Google Scholar : PubMed/NCBI
10	Yager JD and Davidson NE: Estrogen carcinogenesis in breast cancer. N Engl J Med. 354:270–282. 2006. View Article : Google Scholar : PubMed/NCBI
11	Zhao Z, Chen C, Liu Y and Wu C: 17β-Estradiol treatment inhibits breast cell proliferation, migration and invasion by decreasing MALAT-1 RNA level. Biochem Biophys Res Commun. 445:388–393. 2014. View Article : Google Scholar : PubMed/NCBI
12	Lamb R, Lehn S, Rogerson L, Clarke RB and Landberg G: Cell cycle regulators cyclin D1 and CDK4/6 have estrogen receptor-dependent divergent functions in breast cancer migration and stem cell-like activity. Cell Cycle. 12:2384–2394. 2013. View Article : Google Scholar : PubMed/NCBI
13	Al-Hajj M, Wicha MS, Benito-Hernandez A, Morrison SJ and Clarke MF: Prospective identification of tumorigenic breast cancer cells. Proc Natl Acad Sci USA. 100:3983–3988. 2003. View Article : Google Scholar : PubMed/NCBI
14	Livak KJ and Schmittgen TD: Analysis of relative gene expression data using real-time quantitative PCR and the 2(-Delta Delta C(T)) method. Methods. 25:402–408. 2001. View Article : Google Scholar : PubMed/NCBI
15	Miyoshi Y, Murase K, Saito M, Imamura M and Oh K: Mechanisms of estrogen receptor-α upregulation in breast cancers. Med Mol Morphol. 43:193–196. 2010. View Article : Google Scholar : PubMed/NCBI
16	Tyson JJ, Baumann WT, Chen C, Verdugo A, Tavassoly I, Wang Y, Weiner LM and Clarke R: Dynamic modelling of oestrogen signalling and cell fate in breast cancer cells. Nat Rev Cancer. 11:523–532. 2011. View Article : Google Scholar : PubMed/NCBI
17	Berger CE, Qian Y, Liu G, Chen H and Chen X: p53, a target of estrogen receptor (ER) α, modulates DNA damage-induced growth suppression in ER-positive breast cancer cells. J Biol Chem. 287:30117–30127. 2012. View Article : Google Scholar : PubMed/NCBI
18	Platet N, Cathiard AM, Gleizes M and Garcia M: Estrogens and their receptors in breast cancer progression: A dual role in cancer proliferation and invasion. Crit Rev Oncol Hematol. 51:55–67. 2004. View Article : Google Scholar : PubMed/NCBI
19	Takahashi K and Yamanaka S: Induction of pluripotent stem cells from mouse embryonic and adult fibroblast cultures by defined factors. Cell. 126:663–676. 2006. View Article : Google Scholar : PubMed/NCBI