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HNF-4α 通过 mir-122-adam17 通路抑制肝癌细胞增殖。

HNF-4α inhibits hepatocellular carcinoma cell proliferation through mir-122-adam17 pathway.

机构信息

Department of Hepatobiliary and Pancreatic Surgery, The Second Affiliated Hospital of Jilin University, Changchun, Jilin, China.

Department of Pharmacology, College of Basic Medical Sciences, Jilin University, Changchun, China.

出版信息

PLoS One. 2020 Mar 25;15(3):e0230450. doi: 10.1371/journal.pone.0230450. eCollection 2020.

DOI:10.1371/journal.pone.0230450
PMID:32210451
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7094838/
Abstract

Hepatocellular carcinoma (HCC) is one of the most common human cancers, its prevalence and severity need us to discover novel early diagnostic biomarkers and new therapeutic strategies. MicroRNA-122 is the most abundant microRNA in the liver, and acts as a tumor suppressor and represses HCC development. In our study we showed that HNF-4α and MiR-122 were down-regulated significantly in hepatocellular carcinoma. Over-expression of HNF-4α inhibit hepatocellular carcinoma cells proliferation. And miR-122 is one of the downstream effector of HNF-4α. Up-regulated miR-122 inhibited hepatocellular carcinoma cells proliferation through regulating ADAM17. Collectively, our results suggested that HNF-4α could inhibit hepatocellular carcinoma proliferation with miR-122 being a downstream target of it. And miR-122 would inhibit hepatocellular carcinoma proliferation by regulating ADAM17 signal pathway.

摘要

肝细胞癌(HCC)是最常见的人类癌症之一,其普遍性和严重性需要我们发现新的早期诊断生物标志物和新的治疗策略。miR-122 是肝脏中最丰富的 microRNA,作为肿瘤抑制因子,抑制 HCC 的发展。在我们的研究中,我们表明 HNF-4α 和 miR-122 在肝细胞癌中显著下调。HNF-4α 的过表达抑制肝癌细胞的增殖。miR-122 是 HNF-4α 的下游效应物之一。上调的 miR-122 通过调节 ADAM17 抑制肝癌细胞的增殖。总之,我们的结果表明 HNF-4α 可以通过 miR-122 抑制肝癌细胞的增殖,miR-122 是其下游靶点。miR-122 通过调节 ADAM17 信号通路抑制肝癌细胞的增殖。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/27cd/7094838/4075cdadeddb/pone.0230450.g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/27cd/7094838/bb17a8e74e8f/pone.0230450.g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/27cd/7094838/0d97469270e3/pone.0230450.g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/27cd/7094838/68f1d57610f0/pone.0230450.g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/27cd/7094838/4075cdadeddb/pone.0230450.g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/27cd/7094838/bb17a8e74e8f/pone.0230450.g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/27cd/7094838/0d97469270e3/pone.0230450.g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/27cd/7094838/68f1d57610f0/pone.0230450.g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/27cd/7094838/4075cdadeddb/pone.0230450.g004.jpg

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