Conclusion
MIR503HG inhibits NSCLC cell proliferation by inducing cell cycle arrest through the downregulation of cyclin D1.
Methods
MIR503HG expression in paired cancer and non-cancer tissues from NSCLC patients was analyzed by RT-qPCR. The interaction between cyclin D1 and MIR503HG was analyzed by overexpression experiments. Cell cycle analysis was performed by flow cytometry. Cell proliferation was analyzed by CCK-8 assay.
Results
MIR503HG was downregulated in NSCLC and low levels of MIR503HG were associated with poor survival. In contrast, cyclin D1 was upregulated in NSCLC, and cyclin D1 and MIR503HG were inversely correlated. In NSCLC cells, overexpression experiments revealed that MIR503HG functioned as an upstream inhibitor of cyclin D1. MIR503HG overexpression led to G1 cell cycle arrest, while overexpression of cyclin D1 attenuated the effects of MIR503HG overexpression. Similarly, MIR503HG overexpression resulted in reduced cell proliferation rate, while overexpression of cyclin D1 caused the increased cell proliferation rate and attenuated effects of MIR503HG overexpression.