Knockdown of lncRNA MIR503HG suppresses proliferation and promotes apoptosis of non-small cell lung cancer cells by regulating miR-489-3p and miR-625-5p.

The long noncoding RNA (lncRNA) MIR503HG has been shown to play an important role in cancer development. The aim of the present study was to investigate the potential roles of MIR503HG in the proliferation and apoptosis of non-small cell lung cancer cell (NSCLC). We used short hairpin RNA (shRNA) against MIR503HG to knock down and vector containing full length of MIR503HG to overexpress MIR503HG in NSCLC cells. The expression of MIR503HG in NSCLC tissues and cells was detected and the effects of MIR503HG on the cell proliferation and apoptosis were determined. Results showed that the expression of MIR503HG was significantly upregulated in NSCLC tissues compared with adjacent tissues. We found that downregulation of MIR503HG could clearly suppressed cell proliferation and cell cycle progression. Moreover, MIR503HG knockdown also promoted apoptosis of NSCLC cells. As expected, overexpression of MIR503HG significantly promoted cell proliferation and inhibited cell apoptosis in NSCLC NCI-H1975 cells. We predicted and verified miR-489-3p and miR-625-5p as the direct targets of MIR503HG by bioinformatics analysis and luciferase reporter assay. Mechanically, MIR503HG negatively regulated miR-489-3p and miR-625-5p expressions in NSCLC cells. Moreover, downregulation of miR-489-3p and miR-625-5p weaken the decreased cell proliferation and increased apoptosis of A549 cells after MIR503HG knocking down. In conclusion, knockdown of MIR503HG suppressed proliferation and promoted apoptosis of NSCLC cells through regulating miR-489-3p and miR-625-5p. Our findings of this study suggested that MIR503HG could be a potential therapeutic target for NSCLC development.