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微小RNA-139-3p通过抑制膜联蛋白A2受体抑制肝细胞癌的肿瘤生长和转移。

MicroRNA-139-3p Suppresses Tumor Growth and Metastasis in Hepatocellular Carcinoma by Repressing ANXA2R.

作者信息

Zou Zeng Cheng, Dai Min, Huang Zeng Yin, Lu Yi, Xie He Ping, Li Yi Fang, Li Yue, Tan Ying, Wang Feng Lin

机构信息

Department of Integrated Traditional and Western Medicine, The Third Affiliated Hospital of SunYat-sen University, Guangzhou, P.R. China.

Department of Oncology Guangdong Provincial Hospital of Traditional Chinese Medicine, Guangzhou, P.R. China.

出版信息

Oncol Res. 2018 Oct 17;26(9):1391-1399. doi: 10.3727/096504018X15178798885361. Epub 2018 Feb 8.

DOI:10.3727/096504018X15178798885361
PMID:29422116
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7844686/
Abstract

The direct roles of miR-139-3p on hepatocellular carcinoma (HCC) cell growth and metastasis remain poorly understood. We attempted to demonstrate the regulatory role of miR-139-3p in HCC progression and its underlying mechanisms. Here we showed that miR-139-3p expression was significantly reduced in the HCC tissues compared to paratumor tissues. Exogenous overexpression of miR-139-3p inhibited the migration and invasion of HCC cells, whereas downregulation of miR-139-3p was able to induce HCC HepG2 and SNU-449 cell migration and invasion. In addition, miR-139-3p inhibited HCC growth and lung metastasis in an in vivo mouse model, which is mainly regulated by annexin A2 receptor (ANXA2R). Finally, we identified that the expression of miR-139-3p was inversely correlated with ANXA2R expression in human HCC tissue. All these results demonstrated that miR-139-3p inhibited the metastasis process in HCC by downregulating ANXA2R expression.

摘要

miR-139-3p对肝细胞癌(HCC)细胞生长和转移的直接作用仍知之甚少。我们试图证明miR-139-3p在HCC进展中的调节作用及其潜在机制。在此我们表明,与癌旁组织相比,miR-139-3p在HCC组织中的表达显著降低。外源性过表达miR-139-3p可抑制HCC细胞的迁移和侵袭,而miR-139-3p的下调能够诱导HCC HepG2和SNU-449细胞的迁移和侵袭。此外,在体内小鼠模型中,miR-139-3p抑制HCC生长和肺转移,这主要由膜联蛋白A2受体(ANXA2R)调节。最后,我们确定在人类HCC组织中,miR-139-3p的表达与ANXA2R的表达呈负相关。所有这些结果表明,miR-139-3p通过下调ANXA2R的表达抑制HCC的转移过程。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/be38/7844686/48cde8f46cce/OR-26-1391-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/be38/7844686/54019a4dfabd/OR-26-1391-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/be38/7844686/214584846229/OR-26-1391-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/be38/7844686/73e57788757c/OR-26-1391-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/be38/7844686/0bb9a97d267f/OR-26-1391-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/be38/7844686/48cde8f46cce/OR-26-1391-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/be38/7844686/54019a4dfabd/OR-26-1391-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/be38/7844686/214584846229/OR-26-1391-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/be38/7844686/73e57788757c/OR-26-1391-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/be38/7844686/0bb9a97d267f/OR-26-1391-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/be38/7844686/48cde8f46cce/OR-26-1391-g005.jpg

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