Overexpression of ERα inhibits proliferation and invasion of MKN28 gastric cancer cells by suppressing β-catenin
| Autor: | Jianguo Shen, Chenpu Xu, Jufeng Guo, Shuduo Xie, Linbo Wang, Chaoyang Xu, Rongyue Teng, Ziduo Li, Jichun Zhou, Qinchuan Wang |
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| Rok vydání: | 2013 |
| Předmět: |
Cancer Research
Cell Survival Cell Estrogen receptor Apoptosis Adenocarcinoma Biology Cell Movement Stomach Neoplasms Cell Line Tumor medicine Humans Neoplasm Invasiveness beta Catenin Cell Proliferation Oncogene Cell growth Estrogen Receptor alpha Cancer General Medicine Cell cycle medicine.disease G1 Phase Cell Cycle Checkpoints Cell biology Gene Expression Regulation Neoplastic medicine.anatomical_structure Oncology Cancer cell Estrogen receptor alpha |
| Zdroj: | Oncology Reports. 30:1622-1630 |
| ISSN: | 1791-2431 1021-335X |
| Popis: | The relationship between estrogen receptor (ER)α and patient prognosis has been identified in gastric cancer; however, the definite role of ERα in gastric cancer remains to be fully elucidated. The aim of the present in vitro study was to investigate the impact of ERα on cell proliferation, migration and invasion in gastric cancer cell lines. We investigated the biological effect of ERα overexpression on gastric carcinoma cells. An MKN28 gastric cancer cell line stably overexpressing ERα was established. The effect of ERα overexpression on cell growth was assessed by evaluating cell survival, colony formation, cell cycle progression and apoptosis. Cell migration and invasion were detected by Transwell migration/invasion assays. The protein levels of several potentially involved genes were determined by western blotting to elucidate the underlying molecular mechanisms. The Student's t-test was used to determine the statistical differences between various experimental and control groups, and one-way ANOVA test was used to determine the difference between three or more groups. The results showed that ERα overexpression significantly inhibited cell growth and proliferation, blocked cell entry into the G1/G0 phase and promoted cell apoptosis. In addition, ERα reduced the motility and invasion of gastric cancer cells. These phenotypes may partly be explained by a decrease in β-catenin expression caused by ERα overexpression. ERα overexpression effectively inhibited cell growth and cancer progression by suppressing β-catenin in gastric cancer, identifying ERα as a promising target with therapeutic potential for development of new approaches to treat gastric cancer. |
| Databáze: | OpenAIRE |
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