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首页> 外文期刊>Oncology reports >Downregulation of miR-129-2 by promoter hypermethylation regulates breast cancer cell proliferation and apoptosis
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Downregulation of miR-129-2 by promoter hypermethylation regulates breast cancer cell proliferation and apoptosis

机译:启动子高甲基化下调miR-129-2调节乳腺癌细胞增殖和凋亡

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Aberrant expression of the miR-129 family has been found in several types of cancer, yet its expression and potential biologic role in breast cancer remain largely unknown. In the present study, we found that miR-129-2 was consistently downregulated in the breast cancer specimens and cell lines. Overexpression of miR-129-2-3p markedly suppressed breast cancer cell proliferation and induced its apoptosis. In addition, a luciferase reporter assay revealed that miR-129-2-3p suppressed BCL2L2 expression. Furthermore, BCL2L2 was able to reverse miR-129-2-3p-mediated cell apoptosis, indicating that BCL2L2 plays a crucial role in mediating the tumor-suppressive role of miR-129-2-3p. Moreover, bisulfite DNA sequencing PCR (BSP) analysis identified that promoter hypermethylation was responsible for the downregulation of miR-129-2 in breast cancer. Collectively, our findings indicate that miR-129-2 is downregulated in breast cancer cells by promoter hypermethylation. Moreover, downregulation of miR-129-2 results in BCL2L2 overexpression and disease progression in breast cancer patients.
机译:在几种类型的癌症中都发现了miR-129家族的异常表达,但是在乳腺癌中其表达及其潜在的生物学作用仍然未知。在本研究中,我们发现miR-129-2在乳腺癌标本和细胞系中持续下调。 miR-129-2-3p的过表达显着抑制乳腺癌细胞增殖并诱导其凋亡。另外,萤光素酶报告基因测定显示miR-129-2-3p抑制了BCL2L2表达。此外,BCL2L2能够逆转miR-129-2-3p介导的细胞凋亡,表明BCL2L2在介导miR-129-2-3p的肿瘤抑制作用中起关键作用。此外,亚硫酸氢盐DNA测序PCR(BSP)分析表明,启动子甲基化过高是导致miR-129-2在乳腺癌中下调的原因。总的来说,我们的研究结果表明,miR-129-2在乳腺癌细胞中通过启动子高甲基化被下调。此外,miR-129-2的下调导致乳腺癌患者中BCL2L2的过度表达和疾病进展。

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