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首页> 外文期刊>Cancer Cell >miR-221&222 regulate TRAIL resistance and enhance tumorigenicity through PTEN and TIMP3 downregulation.
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miR-221&222 regulate TRAIL resistance and enhance tumorigenicity through PTEN and TIMP3 downregulation.

机译：miR-221＆222通过下调PTEN和TIMP3来调节TRAIL耐药性并增强致瘤性。

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摘要

Lung and liver cancers are among the most deadly types of cancer. Despite improvements in treatment over the past few decades, patient survival remains poor, underlining the need for development of targeted therapies. MicroRNAs represent a class of small RNAs frequently deregulated in human malignancies. We now report that miR-221&222 are overexpressed in aggressive non-small cell lung cancer and hepatocarcinoma cells, as compared with less invasive and/or normal lung and liver cells. We show that miR-221&222, by targeting PTEN and TIMP3 tumor suppressors, induce TRAIL resistance and enhance cellular migration through the activation of the AKT pathway and metallopeptidases. Finally, we demonstrate that the MET oncogene is involved in miR-221&222 activation through the c-Jun transcription factor.
机译：肺癌和肝癌是最致命的癌症之一。尽管在过去的几十年中治疗方法有所改善，但患者的存活率仍然很差，这强调了开发靶向疗法的必要性。 MicroRNA代表一类经常在人类恶性肿瘤中失活的小RNA。我们现在报道，与侵袭性和/或正常肺和肝细胞相比，miR-221＆222在侵袭性非小细胞肺癌和肝癌细胞中过表达。我们显示，通过靶向PTEN和TIMP3肿瘤抑制物，miR-221＆222可以诱导TRAIL抗性，并通过激活AKT途径和金属肽酶来增强细胞迁移。最后，我们证明MET癌基因通过c-Jun转录因子参与miR-221＆222激活。

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