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Content Provider | World Health Organization (WHO)-Global Index Medicus |
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Author | Jiang, Zhinong Guo, Junlan Shen, Jianguo Jin, Mei Xie, Shuduo Wang, Linbo |
Description | Country affiliation: China Author Affiliation: Jiang Z ( Department of Surgical Oncology, Sir Run Run Shaw Hospital, Zhejiang University College of Medicine, Hangzhou, China.) |
Abstract | INTRODUCTION: Previous studies suggested that estrogen receptor alpha (ER ) plays an important role in the chemoresistance of breast cancers. However, large random trials failed to demonstrate any benefit of the concurrent estrogen antagonist tamoxifen on the chemotherapy efficacy. Thus, in the present study, the importance of the role of ER in the chemoresistance of breast cancer cells was investigated. METHODS: The ER -transfected Bcap37 cells and natural ER -positive T47D breast cancer cells were treated using chemotherapeutic agents with or without 17-beta estradiol (E2) pretreatment. Their viabilities were assessed using 3-[4,5-dimethylthiazol-2-yl]-2,5-diphenyltetrazolium bromide assays. The dead cell rates were determined using propidium iodide dye exclusion tests, and the expression levels of Bcl-2 and Bax were detected through Western blot analysis. The effects of E2 on the growth of breast cancer cells were also determined via cell growth curve and cell cycle analysis. RESULTS: ER activation by E2 increased the sensitivity of natural ER -positive T47D breast cancer cells to chemotherapeutic agents. However, the increase in ER expression in ER -negative Bcap37 breast cancer cells also significantly increased their resistance. These phenomena cannot be explained by asserting that ER mediated the chemoresistance of breast cancer cells by regulating the expression of Bcl-2 and Bax. Our findings show that ER activation upregulated the expression of Bcl-2 in natural ER -positive T47D breast cancer cells, whereas ER activation by E2 downregulated and upregulated the Bcl-2 and Bax expression levels, respectively, in ER -transfected Bcap37 cells. This phenomenon was due to the influence of ER on the growth of breast cancer cells. Specifically, ER activation enhanced the growth of natural ER -positive breast cancer cells and thus increased their sensitivity to chemotherapeutic agents. However, ER activation also inhibited the growth of ER -transfected Bcap37 cells and increased the resistance of cancer cells to chemotherapeutic agents. Chemoresistance of ER -transfected Bcap37 cells was only due to the specific growth inhibition by E2, which is not applicable to common ER -positive breast cancer cells. CONCLUSIONS: Although ER was associated with chemoresistance of breast cancers, ER itself did not mediate this resistance process. |
File Format | HTM / HTML |
ISSN | 03929078 |
e-ISSN | 17569966 |
DOI | 10.1186/1756-9966-31-42 |
Journal | Journal of Experimental & Clinical Cancer Research |
Volume Number | 31 |
Language | English |
Publisher | BioMed Central |
Publisher Date | 2012-05-03 |
Publisher Place | Great Britain (UK) |
Access Restriction | Open |
Subject Keyword | Discipline Oncology Antineoplastic Agents Pharmacology Breast Neoplasms Drug Therapy Metabolism Estrogen Receptor Alpha Genetics Pathology Cell Growth Processes Drug Effects Physiology Cell Line, Tumor Drug Resistance, Neoplasm Estradiol Analogs & Derivatives Estrogen Antagonists Gene Expression Regulation, Neoplastic Proto-oncogene Proteins C-bcl-2 Biosynthesis Transfection Up-regulation Bcl-2-associated X Protein Research Support, Non-u.s. Gov't |
Content Type | Text |
Resource Type | Article |
Subject | Cancer Research Oncology |
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