Effects of lncRNA MEG3 on proliferation and apoptosis of gallbladder cancer cells through regulating NF-κB signaling pathway.

Abstract

To explore the effects of long non-coding ribonucleic acid (lncRNA) maternally expressed gene 3 (MEG3) on proliferation and apoptosis of gallbladder cancer (GBC) cells and its molecular mechanism. The relative expression level of lncRNA MEG3 in GBC cell lines was detected via quantitative Reverse Transcription-Polymerase Chain Reaction (qRT-PCR). The lncRNA MEG3 expression plasmids were constructed, the cell proliferation ability was detected via Cell Counting Kit-8 (CCK-8) assay and colony formation assay, and the apoptosis was detected via flow cytometry. The effects of lncRNA MEG3 expression on endoplasmic reticulum stress (ERS)-related proteins were determined using Western blotting, and the changes in nuclear factor-κB (NF-κB) protein in the nucleus were determined after overexpression of lncRNA MEG3. The expression of lncRNA MEG3 in three kinds of GBC cell lines was lower than that in human immortalized normal biliary epithelial cells (p<0.05). The results of CCK-8 assay and colony formation assay showed that overexpression of lncRNA MEG3 significantly reduced the proliferation rate and colony formation ability of GBC-SD cells compared with negative control (NC) group (p<0.05, p<0.05). According to the results of flow cytometry, the apoptosis rate was higher in lncRNA MEG63 overexpression group compared with that in NC group (p<0.05). Moreover, the ERS-related proteins (MANF, GRP78, and caspase-3) were remarkably upregulated in lncRNA MEG63 overexpression group compared with those in NC group, indicating that ERS is activated by lncRNA MEG63 overexpression. The NF-κB signal in GBC cells was activated by lncRNA MEG3. LncRNA MEG3 activates the NF-κB signal in GBC cells to affect the proliferation and apoptosis of GBC cells.