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上调的微小RNA-16作为肾细胞癌中的一种癌基因。

Upregulated microRNA-16 as an oncogene in renal cell carcinoma.

作者信息

Chen Duqun, Li Yifan, Yu Zuhu, Su Zhengming, Yu Wenshui, Li Yuchi, Yang Shangqi, Gui Yaoting, Ni Liangchao, Lai Yongqing

机构信息

Department of Urology, Peking University Shenzhen Hospital, Shenzhen, Guangdong 518036, P.R. China.

Guangdong and Shenzhen Key Laboratory of Male Reproductive Medicine and Genetics, Institute of Urology, Shenzhen PKU‑HKUST Medical Center, Shenzhen, Guangdong 518036, P.R. China.

出版信息

Mol Med Rep. 2015 Jul;12(1):1399-404. doi: 10.3892/mmr.2015.3496. Epub 2015 Mar 17.

Abstract

MicroRNAs (miRs) are small, endogenous noncoding RNAs that serve a significant function in various biologic processes, including those involved in cancer. The present study aimed to determine the expression and function of miR-16 in renal cell carcinoma (RCC). Quantitative polymerase chain reaction was used to quantify the expression of miR-16 in 48 paired RCC tissues and adjacent normal tissues. The impact of miR-16 on cell proliferation, migration and apoptosis was analyzed by transfecting miR-16 mature molecules into the renal cancer cell lines 786-O and ACHN. The results indicated that miR-16 was significantly upregulated in RCC tissues (P<0.05). Downregulation of miR-16 resulted in reduced cell proliferation and migration and increased levels of apoptosis, while overexpression of miR-16 resulted in accelerated cellular proliferation and migration, suggesting that miR-16 may function as an oncogene in RCC. The present study demonstrated for the first time, to the best of our knowledge, that miR-16 is upregulated in RCC and acts as an oncogene by inducing cellular proliferation, migration and reducing apoptosis. Further study of miR-16 in RCC may clarify the molecular mechanisms of RCC carcinogenesis and aid in the development of novel biomarkers and therapeutic options.

摘要

微小RNA(miR)是一类小型内源性非编码RNA,在包括癌症相关过程在内的各种生物学过程中发挥着重要作用。本研究旨在确定miR-16在肾细胞癌(RCC)中的表达及功能。采用定量聚合酶链反应对48对RCC组织及相邻正常组织中miR-16的表达进行定量。通过将miR-16成熟分子转染至肾癌细胞系786-O和ACHN中,分析miR-16对细胞增殖、迁移和凋亡的影响。结果表明,RCC组织中miR-16显著上调(P<0.05)。下调miR-16导致细胞增殖和迁移减少,凋亡水平增加,而miR-16过表达则导致细胞增殖和迁移加速,提示miR-16可能在RCC中作为癌基因发挥作用。据我们所知,本研究首次证明miR-16在RCC中上调,并通过诱导细胞增殖、迁移和减少凋亡而发挥癌基因作用。对RCC中miR-16的进一步研究可能会阐明RCC致癌的分子机制,并有助于开发新的生物标志物和治疗方案。

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