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首页> 外文期刊>Journal of cellular physiology. >miR-145 promotes miR-133b expression through c-myc and DNMT3A-mediated methylation in ovarian cancer cells
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miR-145 promotes miR-133b expression through c-myc and DNMT3A-mediated methylation in ovarian cancer cells

机译：mir - 145促进mir - 133 b通过原癌基因表达并在卵巢癌DNMT3A-mediated甲基化细胞

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摘要

Ovarian cancer presents as malignant tumors in the female reproductive system with high mortality. MicroRNAs are involved in the progression of ovarian cancer; however, the regulatory relationship among miRs remains unclear. In our study, we verified that both miR-145 and miR-133b messenger RNA (mRNA) levels in ovarian cancer tissues were lower than in normal ovarian tissues, and their mRNA level in serum of patients with ovarian cancer was reduced. We demonstrated miR-145 targeted c-myc, and c-myc interacted physically with DNMT3A in ovarian cancer cells. We confirmed that c-myc recruited DNMT3A to the miR-133b promoter. miR-133b overexpression also inhibited target gene PKM2 expression along with the Warburg effect. Our results indicate that miR-145 inhibited the Warburg effect through miR-133b/PKM2 pathways, which may improve approaches to ovarian cancer diagnosis and treatment.
机译：卵巢癌的恶性肿瘤女性生殖系统与高死亡率。小分子核糖核酸参与的发展卵巢癌;大鹏之间的关系尚不清楚。研究中,我们验证了mir - 145和mir - 133 b信使核糖核酸(mRNA)水平在卵巢癌组织是低于正常的卵巢组织和血清的mRNA水平卵巢癌患者被降低。证明mir - 145有针对性的原癌基因和原癌基因身体互动DNMT3A卵巢癌细胞。DNMT3A mir - 133 b子。超表达PKM2也抑制目标基因随着Warburg效应表达式。结果表明,mir - 145抑制了Warburg效应通过mir - 133 b / PKM2途径,这可能会提高卵巢癌的方法诊断和治疗。

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