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Long non‐coding RNA myocardial infarction associated transcript promotes the proliferation of cholangiocarcinoma cells by targeting miR‐551b‐3p/CCND1 axis
Author(s) -
Chang Weiping,
Wang Yuan,
Li WenZhi,
Geng Zhimin
Publication year - 2020
Publication title -
clinical and experimental pharmacology and physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.752
H-Index - 103
eISSN - 1440-1681
pISSN - 0305-1870
DOI - 10.1111/1440-1681.13283
Subject(s) - gene knockdown , cyclin d1 , cancer research , cell growth , apoptosis , long non coding rna , gene silencing , biology , cell cycle , downregulation and upregulation , cyclin e1 , cell culture , ectopic expression , gene , genetics
Abstract Accumulating reports have demonstrated that long non‐coding RNAs (lncRNAs) play critical roles in the occurrence and metastasis of cholangiocarcinoma (CCA). LncRNA myocardial infarction associated transcript (MIAT) has been widely reported in hepatocellular carcinoma, pancreatic cancer and colorectal cancer, but the relationship between MIAT and CCA progression has not yet been investigated. In the present study, we found that the expression of MIAT in CCA tissues was prominently higher than that in normal bile duct tissues. Moreover, TCGA‐CHOL data in the GEPIA platform further revealed the upregulated expression of MIAT in CCA tissues. Additionally, quantitative real‐time PCR results showed that MIAT expression was increased in CCA cell lines compared to the human intrahepatic biliary epithelial cell line. Functionally, MIAT knockdown significantly inhibited cell proliferation and induced G0/G1 phase arrest as well as apoptosis in HuCCT‐1 and QBC939 cells. Conversely, ectopic expression of MIAT obviously facilitated the proliferation, cell cycle progression and apoptosis resistance of RBE cells. Mechanistically, MIAT directly interacted with miR‐551b‐3p and inversely modulated miR‐551‐3p level in CCA cells. Furthermore, MIAT knockdown reduced the expression of cyclin D1 (CCND1), which was rescued by miR‐551b‐3p silencing in HuCCT‐1 cells. Importantly, CCND1 restoration partially reversed MIAT knockdown‐induced proliferation inhibition, G0/G1 phase arrest and apoptosis in HuCCT‐1 cells. In conclusion, MIAT was frequently overexpressed in CCA. MIAT contributed to the growth of CCA cells by targeting miR‐551b‐3p/CCND1 axis.