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首页> 外文期刊>Molecular medicine reports >microRNA-206 overexpression inhibits cellular proliferation and invasion of estrogen receptor α-positive ovarian cancer cells
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microRNA-206 overexpression inhibits cellular proliferation and invasion of estrogen receptor α-positive ovarian cancer cells

机译:microRNA-206过表达抑制雌激素受体α阳性卵巢癌细胞的细胞增殖和侵袭

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摘要

The expression levels of estrogen receptor (ER α) are closely associated with estrogen-dependent growth, invasion and response to endocrine therapy in ERα-positive ovarian cancer. However, the underlying regulatory mechanisms remain to be fully understood. Previous studies have demonstrated that ERα is a direct target of microRNA (miR)-206. miR-206 has been found to be an important tumor suppressor in several cancer types, including ovarian, gastric and laryngeal cancer. However, the specific role of miR-206 in ovarian cancer remains unclear. The aim of the present study was to investigate the role of miR-206 in ER-a positive ovarian cancer in vitro. The present study demonstrated that miR-206 is significantly downregulated in ERα-positive but not ERα-negative ovarian cancer tissues, compared with normal ovarian epithelium tissue. It was also found that the expression of miR-206 was decreased in ERα-positive ovarian cancer cell lines, CAOV-3 and BG-1, compared with normal ovarian epithelium tissues. This suggests that miR-206 may play a role in ERα-positive ovarian cancer cells via an estrogen-dependent mechanism. Further analysis revealed that 17β-E2 treatment significantly promoted cellular proliferation and invasion of estrogen-dependent CAOV-3 and BG-1 cells, which could be reversed by the introduction of miR-206 mimics. In conclusion, the present study suggests that miR-206 has an inhibitory role in estrogen-dependent ovarian cancer cells. Thus, miR-206 may be a promising candidate for the endocrine therapy of ERα-positive ovarian cancer.
机译:雌激素受体(ERα)的表达水平与雌激素依赖性生长,侵袭和对ERα阳性卵巢癌的内分泌治疗的反应密切相关。但是,潜在的监管机制仍有待充分理解。先前的研究表明,ERα是microRNA(miR)-206的直接靶标。已发现miR-206在包括卵巢癌,胃癌和喉癌在内的多种癌症类型中是重要的肿瘤抑制因子。但是,miR-206在卵巢癌中的具体作用仍不清楚。本研究的目的是研究miR-206在体外ER-a阳性卵巢癌中的作用。本研究表明,与正常卵巢上皮组织相比,miR-206在ERα阳性而不是ERα阴性卵巢癌组织中显着下调。还发现,与正常卵巢上皮组织相比,ERα-阳性卵巢癌细胞系CAOV-3和BG-1中miR-206的表达降低。这表明miR-206可能通过雌激素依赖性机制在ERα阳性卵巢癌细胞中发挥作用。进一步的分析表明,17β-E2处理可显着促进雌激素依赖性CAOV-3和BG-1细胞的细胞增殖和侵袭,这可以通过引入miR-206模拟物来逆转。总之,本研究表明,miR-206在雌激素依赖性卵巢癌细胞中具有抑制作用。因此,miR-206可能是ERα阳性卵巢癌的内分泌治疗的有希望的候选者。

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