PUMA is a novel target of miR-221/222 in human epithelial cancers
PUMA is a novel target of miR-221/222 in human epithelial cancers
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PUMA 是人类上皮癌中 miR-221/222 的新靶点。
DOI：
10.3892/ijo_00000816
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发表时间：
2010-12-01
影响因子：
5.2
通讯作者：
Kang, Chunsheng
中科院分区：
文献类型：
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作者：
Zhang, Chunzhi;Zhang, Junxia;Kang, Chunsheng
miR-221和miR-222（miR-221/222）在人类上皮癌中频繁上调。然而，miR-221/222参与致癌作用的机制尚未得到广泛研究。在这里，我们发现miR-221/222的减少抑制了人上皮癌细胞（A549肺癌和MCF-7乳腺癌细胞）的细胞增殖并诱导了细胞介导的凋亡。生物信息学和荧光素酶报告基因分析显示，miR-221/222通过直接靶向3 'UTR内的结合位点共调节p53上调的凋亡调节因子（p53）表达。总之，这些研究结果表明，在这些上皮癌中，miR-221/222作为内源性凋亡调节因子发挥作用，而miR-221/222的直接靶点是miR-221/222。
miR-221 and miR-222 (miR-221/222) are frequently up-regulated in human epithelial cancers. However, the mechanism of miR-221/222 action involved in carcinogenesis has not been extensively studied. Here, we found that reduction of miR-221/222 inhibited cell proliferation and induced mitochondrial-mediated apoptosis in human epithelial cancer cells (A549 lung cancer and MCF-7 breast cancer cells). Bioinformatics and luciferase reporter assays showed that miR-221/222 co-modulated the p53 upregulated modulator of apoptosis (PUMA) expression by directly targeting the binding site within the 3'UTR. Together, these findings suggest that PUMA is a direct target of miR-221/222 that functions as an endogenous apoptosis regulator in these epithelial cancers.