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lncRNA DRHC inhibits proliferation and invasion in hepatocellular carcinoma via c‐Myb‐regulated MEK/ERK signaling
Author(s) -
Zhuang Runzhou,
Zhang Xuanyu,
Lu Di,
Wang Jianguo,
Zhuo Jianyong,
Wei Xuyong,
Ling Qi,
Xie Haiyang,
Zheng Shusen,
Xu Xiao
Publication year - 2019
Publication title -
molecular carcinogenesis
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.254
H-Index - 97
eISSN - 1098-2744
pISSN - 0899-1987
DOI - 10.1002/mc.22934
Subject(s) - biology , trametinib , mapk/erk pathway , cancer research , long non coding rna , hepatocellular carcinoma , cell growth , myb , mek inhibitor , signal transduction , microbiology and biotechnology , downregulation and upregulation , gene expression , gene , genetics
Accumulating evidence indicates that long non‐coding RNAs (lncRNAs) play a crucial role in hepatocellular carcinoma (HCC). Here, we reported a novel lncRNA, CTC‐505O3 (lncRNA DRHC), that was downregulated in HCC and its low expression was associated with dismal survival. Gain‐of‐function studies indicated that it inhibited proliferation, migration, invasion, and epithelial‐mesenchymal transition (EMT) in HCC cell lines in vitro. lncRNA DRHC also inhibited tumorigenicity in vivo. In mechanistic experiments, GO analysis based on NGS indicated that MAPK signaling was most affected. The result was confirmed by Western blot and this effect was abolished either by MEK1/2 specific inhibitor Trametinib or ERK1/2 inhibitor SCH772984. In addition, differences in proliferation and invasion were abrogated by Trametinib. Moreover, we found that lncRNA DRHC interacted with MYBBP1A and modulated MEK/ERK signaling via c‐Myb. Taken together, our findings indicate that the lncRNA DRHC play a key role in HCC progression and may serve as a novel therapeutic target.