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

OBJECTIVE: To explore the effects of long non-coding ribonucleic acid (IncRNA) maternally expressed gene 3 (MEG3) on proliferation and apoptosis of gallbladder cancer (GBC) cells and its molecular mechanism. MATERIALS AND METHODS: The relative expression level of IncRNA MEG3 in GBC cell lines was detected via quantitative Reverse Transcription-Polymerase Chain Reaction (qRT-PCR). The IncRNA 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 IncRNA MEG3 expression on endoplasmic reticulum stress (ERS)-related proteins were determined using Western blotting, and the changes in nuclear factor-kappa B (NF-kappa B) protein in the nucleus were determined after overexpression of IncRNA MEG3. RESULTS: The expression of IncRNA 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 IncRNA 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 IncRNA 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 IncRNA MEG63 overexpression group compared with those in NC group, indicating that ERS is activated by IncRNA MEG63 overexpression. The NF-kappa B signal in GBC cells was activated by IncRNA MEG3. CONCLUSIONS: LncRNA MEG3 activates the NF-kappa B signal in GBC cells to affect the proliferation and apoptosis of GBC cells.