HDAC2 promotes the EMT of colorectal cancer cells and via the modular scaffold function of ENSG00000274093.1

HDAC2 促进结直肠癌细胞的 EMT 并通过 ENSG00000274093.1 的模块化支架功能

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作者:Zhi-Peng Qi, Ayimukedisi Yalikong, Jia-Wei Zhang, Shi-Lun Cai, Bing Li, Sun Di, Zhen-Tao Lv, En-Pan Xu, Yun-Shi Zhong, Ping-Hong Zhou

Abstract

Histone deacetylase 2 (HDAC2), a member of the Histone deacetylase family, plays a vital role in various carcinomas. In this study, we identified that HDAC2 expression levels are associated with liver metastasis, higher T stages and poor prognosis in colorectal cancer. HDAC2 down-regulation via lentivirus-mediated expression of HDAC2-targeting shRNA reduced the in vitro migration and invasion ability of HCT116 cell as well as their liver metastasis in nude mouse xenografts. Mechanistically, HDAC2 promotes epithelial-mesenchymal transition (EMT) in colorectal cancer cells by combining HDAC1 with EZH2 (a key histone methyltransferase), possibly through the modular scaffold function of a new lncRNA, ENSG00000274093.1. HDAC2 thus appears to promote CRC cell migration and invasion through binding HDAC1 and EZH2 via ENSG00000274093.1.

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