HDAC2 promotes the EMT of colorectal cancer cells and via the modular scaffold function of ENSG00000274093.1
Zhipeng Qi, Ayimukedisi Yalikong, Jiawei Zhang, Shi‐Lun Cai, Bing Li, Sun Di, Zhen‐Tao Lv, En‐Pan Xu, Yunshi 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.