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IGF2BP2通过一种依赖于m6A-FEN1的机制促进肝癌生长。

IGF2BP2 Promotes Liver Cancer Growth Through an m6A-FEN1-Dependent Mechanism.

作者信息

Pu Jian, Wang Jianchu, Qin Zebang, Wang Anmin, Zhang Ya, Wu Xianjian, Wu Yi, Li Wenchuan, Xu Zuoming, Lu Yuan, Tang Qianli, Wei Huamei

机构信息

Department of General Surgery, Affiliated Hospital of Youjiang Medical University for Nationalities, Guangxi, China.

Department of Hepatobiliary Surgery, Affiliated Hospital of Youjiang Medical University for Nationalities, Guangxi, China.

出版信息

Front Oncol. 2020 Nov 2;10:578816. doi: 10.3389/fonc.2020.578816. eCollection 2020.

DOI:10.3389/fonc.2020.578816
PMID:33224879
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7667992/
Abstract

Hepatocellular carcinoma (HCC) is one of the most common malignant tumors in China. N6-methyladenosine (m6A) plays an important role in posttranscriptional gene regulation. METTL3 and IGF2BP2 are key genes in the m6A signal pathway and have recently been shown to play important roles in cancer development and progression. In our work, higher METTL3 and IGF2BP2 expression were found in HCC tissues and were associated with a poor prognosis. In addition, IGF2BP2 overexpression promoted HCC proliferation and . Mechanistically, IGF2BP2 directly recognized and bound to the m6A site on FEN1 mRNA and enhanced FEN1 mRNA stability. Overall, our study revealed that METTL3 and IGF2BP2, acting as an oncogene, maintained FEN1 expression through an m6A-IGF2BP2-dependent mechanism in HCC cells, and indicated a potential biomarker panel for prognostic prediction in liver cancer.

摘要

肝细胞癌（HCC）是中国最常见的恶性肿瘤之一。N6-甲基腺苷（m6A）在转录后基因调控中起重要作用。METTL3和IGF2BP2是m6A信号通路中的关键基因，最近已证明它们在癌症发生和发展中起重要作用。在我们的研究中，发现HCC组织中METTL3和IGF2BP2表达较高，且与预后不良相关。此外，IGF2BP2过表达促进HCC增殖以及……机制上，IGF2BP2直接识别并结合FEN1 mRNA上的m6A位点，增强FEN1 mRNA稳定性。总体而言，我们的研究表明，METTL3和IGF2BP2作为癌基因，通过m6A-IGF2BP2依赖性机制维持HCC细胞中FEN1的表达，并为肝癌预后预测指明了一个潜在的生物标志物组合。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/13c4/7667992/040be0eb0c77/fonc-10-578816-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/13c4/7667992/a1032d9a9ee1/fonc-10-578816-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/13c4/7667992/9ec029f05bc8/fonc-10-578816-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/13c4/7667992/f3674482299f/fonc-10-578816-g003.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/13c4/7667992/efc9f36b8efb/fonc-10-578816-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/13c4/7667992/040be0eb0c77/fonc-10-578816-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/13c4/7667992/a1032d9a9ee1/fonc-10-578816-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/13c4/7667992/9ec029f05bc8/fonc-10-578816-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/13c4/7667992/f3674482299f/fonc-10-578816-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/13c4/7667992/2980514834be/fonc-10-578816-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/13c4/7667992/efc9f36b8efb/fonc-10-578816-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/13c4/7667992/040be0eb0c77/fonc-10-578816-g006.jpg

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