Open AccessLINC00238 inhibits hepatic carcinoma progression by activating TMEM106C‑mediated apoptosis pathway
Author(s) -
Caihua Jiang,
Feng Li,
Meng Yang,
Jianping Duan,
Jianming Lai,
Shulun Sun,
ShaoHua Fan
Publication year - 2021
Publication title -
molecular medicine reports
Language(s) - Uncategorized
Resource type - Journals
SCImago Journal Rank - 0.727
H-Index - 56
eISSN - 1791-3004
pISSN - 1791-2997
DOI - 10.3892/mmr.2021.12397
Subject(s) - apoptosis , oncogene , cell cycle , cancer research , biology , atf3 , cell growth , cell , microbiology and biotechnology , gene expression , gene , promoter , biochemistry , genetics
The present study aimed to explore the regulatory mechanism of long intergenic non‑protein coding (LINC)00238 in hepatocellular carcinoma (HCC). LINC00238 expression in HCC tissues and cell lines was measured using reverse transcription‑quantitative PCR. LncTar was used to predict the binding sites between LINC00238 and transmembrane protein 106C (TMEM106C). Survival analysis of LINC00238, TMEM106C and activating transcription factor 3 (ATF3) in patients with HCC was performed based on TCGA data. The proliferation, apoptosis, migration, and invasion of HCC cells were measured by 3‑(4,5‑dimethylthiazol‑2‑yl)‑5‑(3‑carboxymethoxyphenyl)‑2‑(4‑sulfophenyl)‑2H‑tetrazolium assay, ow cytometer, wound healing and Transwell assays, respectively. LINC00238 promoted apoptosis and inhibited proliferation, migration and invasion of HCC cells. LINC00238 was downregulated in HCC. TMEM106C was a target of LINC00238 and TMEM106C expression was negatively regulated by LINC00238. TMEM106C suppressed the apoptosis pathway and decreased the expression of caspase‑7, tissue inhibitor of metalloproteinase 2, programmed cell death 4 and ATF3. Notably, ATF3 was the upstream promoter of LINC00238 and positively regulated LINC00238 expression. In conclusion, LINC00238 inhibited HCC progression by inhibiting TMEM106 expression and activating the TMEM106C‑mediated apoptosis pathway.