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通过驱动上皮-间质转化促进肝细胞癌进展

Accelerates Hepatocellular Carcinoma Progression by Driving the Epithelial-to-Mesenchymal Transition.

作者信息

Tong Hui, Liu Xiaohui, Li Tao, Qiu Weihua, Peng Chenghong, Shen Baiyong, Zhu Zhecheng

机构信息

Department of General Surgery, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 200025, People's Republic of China.

CNRS-LIA124, Sino-French Research Center for Life Sciences and Genomics, State Key Laboratory of Medical Genomics, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 200025, People's Republic of China.

出版信息

Onco Targets Ther. 2020 May 8;13:3931-3942. doi: 10.2147/OTT.S237804. eCollection 2020.

DOI:10.2147/OTT.S237804
PMID:32440156
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7217318/
Abstract

INTRODUCTION

A poor prognosis owing to cancer invasion and metastasis, hepatocellular carcinoma (HCC) is one of the leading causes of malignancy deaths worldwide. A dominant epithelial-to-mesenchymal transition or EMT function in tumour metastasis is substantially evidenced. Prior reports identified a likely correlation of the nuclear hormone receptor with HCC progression, but the underlying molecular mechanisms and role of invasion and metastasis are still to be adequately documented.

METHODS

We carried out PROGgeneV2 platform database analysis and compared expression in HCC tissues with that in adjacent noncancerous tissues by Western blotting. Cell proliferation, invasion, and migration were also assessed using a lentivirus system. Moreover, the relevant signalling proteins were evaluated.

RESULTS

The PROGgeneV2 platform database analysis suggested an upregulated expression related to poor overall survival, or OS, in HCC, with higher levels in HCC, compared to the adjoining non-cancerous tissue. Depleting decreased HCC cell proliferation, migration and invasion in vitro, whilst in vivo downregulation revealed fewer metastatic nodules in the lungs. Furthermore, knockdown amplified epithelial marker, namely E-cadherin expressions, and decreased mesenchymal markers, ie, N-cadherin and vimentin expressions, with β-catenin overexpression.

CONCLUSION

is shown to accelerate HCC progression via driving EMT.

摘要

引言

由于癌症侵袭和转移，肝细胞癌（HCC）预后较差，是全球恶性肿瘤死亡的主要原因之一。肿瘤转移中上皮-间质转化（EMT）功能占主导地位已得到充分证实。先前的报道确定了核激素受体与HCC进展可能存在相关性，但其潜在的分子机制以及侵袭和转移的作用仍有待充分记录。

方法

我们进行了PROGgeneV2平台数据库分析，并通过蛋白质印迹法比较了HCC组织与相邻非癌组织中的表达情况。还使用慢病毒系统评估了细胞增殖、侵袭和迁移。此外，对相关信号蛋白进行了评估。

结果

PROGgeneV2平台数据库分析表明，HCC中表达上调与总体生存率（OS）较差相关，与相邻非癌组织相比，HCC中的水平更高。在体外，耗尽可降低HCC细胞的增殖、迁移和侵袭，而在体内下调则显示肺中的转移结节减少。此外，敲低可增强上皮标志物E-钙黏蛋白的表达，并降低间质标志物N-钙黏蛋白和波形蛋白的表达，同时β-连环蛋白过表达。

结论

研究表明可通过驱动EMT加速HCC进展。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cdb0/7217318/8aa5ffe11c47/OTT-13-3931-g0007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cdb0/7217318/4a245371b52a/OTT-13-3931-g0001.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cdb0/7217318/7dfed7efe47a/OTT-13-3931-g0006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cdb0/7217318/8aa5ffe11c47/OTT-13-3931-g0007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cdb0/7217318/4a245371b52a/OTT-13-3931-g0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cdb0/7217318/b3daa207e94d/OTT-13-3931-g0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cdb0/7217318/3db6820c913b/OTT-13-3931-g0003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cdb0/7217318/16b5c0313d81/OTT-13-3931-g0004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cdb0/7217318/0ac481507b88/OTT-13-3931-g0005.jpg
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