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首页> 外文期刊>Molecular medicine reports >Catalpol suppresses proliferation and facilitates apoptosis of MCF-7 breast cancer cells through upregulating microRNA-146a and downregulating matrix metalloproteinase-16 expression
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Catalpol suppresses proliferation and facilitates apoptosis of MCF-7 breast cancer cells through upregulating microRNA-146a and downregulating matrix metalloproteinase-16 expression

机译:Catalpol通过上调microRNA-146a和下调基质金属蛋白酶16表达来抑制MCF-7乳腺癌细胞的增殖并促进其凋亡

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摘要

Breast cancer is the most common malignancy in women, and was the second highest cause of mortality in women in 2013. Matrix metalloproteinase-16 (MMP-16) is an enhancer of the invasion of breast cancer cells. The expression of microRNA-146a (miR-146a) has been reported to be significantly greater in patients with breast cancer compared with healthy controls. Catalpol is one of the main active ingredients of Rehmannia, of which the key pharmacological effects are antitumoral and antiproliferative. The present study was performed to investigate the effect of catalpol on breast cancer and to explore the potential therapeutic mechanisms. Cell proliferation was investigated using an MTT assay, and caspase-3 activity assays and flow cytometry were used to assess apoptosis in MCF-7 breast cancer cells. The expression levels of MMP-16 and miR-146a were investigated using gelatin zymography assays and reverse transcription-quantitative polymerase chain reaction, respectively. In addition, MCF-7 cells were transfected with miR-146a and anti-miR-146a to further investigate the effects of catalpol. The results demonstrated that catalpol reduced proliferation and promoted apoptosis in MCF-7 cells, reducing MMP-16 activity and increasing the expression of miR-146a in MCF-7 cells. This suggests that miR-146a may regulate and control the expression levels of MMP-16 in MCF-7 cells. In conclusion, catalpol suppresses proliferation and facilitates apoptosis of MCF-7 breast cancer cells through upregulating miR-146a and downregulating MMP-16 expression.
机译:乳腺癌是女性中最常见的恶性肿瘤,也是2013年女性死亡率的第二高原因。基质金属蛋白酶-16(MMP-16)是乳腺癌细胞侵袭的增强剂。据报道,与健康对照组相比,乳腺癌患者中microRNA-146a(miR-146a)的表达明显更高。梓醇是熟地黄的主要活性成分之一,其关键药理作用是抗肿瘤和抗增殖。本研究旨在调查梓醇对乳腺癌的作用并探讨潜在的治疗机制。使用MTT测定法研究细胞增殖,并使用caspase-3活性测定法和流式细胞术评估MCF-7乳腺癌细胞的凋亡。分别使用明胶酶谱分析和逆转录定量聚合酶链反应研究了MMP-16和miR-146a的表达水平。此外,用miR-146a和抗miR-146a转染MCF-7细胞,以进一步研究catalpol的作用。结果表明,梓醇减少了MCF-7细胞的增殖并促进了其凋亡,降低了MMP-16活性并增加了MCF-7细胞中miR-146a的表达。这表明miR-146a可能调控MCF-7细胞中MMP-16的表达水平。总之,catalpol通过上调miR-146a和下调MMP-16表达来抑制MCF-7乳腺癌细胞的增殖并促进其凋亡。

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