LINC00238 inhibits hepatic carcinoma progression by activating TMEM106C-mediated apoptosis pathway

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, flow 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.

Automated summary

LINC00238 inhibits HCC progression by inhibiting TMEM106 expression and activating the TMEM106C-mediated apoptosis pathway.