Description:
The objective of this study was to analyze the influence of long non-coding ribonucleic acid PGM5-AS1 on lung cancer cell ferroptosis through microrna-587. To this end, the research team has included the abnormal expression vectors of PGM5-AS1 and microrna-587 were transfected into human lung cancer cell line A549 to detect alterations in cell activity, apoptosis, cell cycle, oxidative stress, iron ion and ferroptosis-associated proteins. The results show silencing PGM5-AS1 or elevating microrna-587 promoted A549 proliferation and invasion, while inhibiting apoptosis and resisting ferroptosis. However, increasing PGM5-AS1 or silencing microrna-587 enhanced A549 apoptosis and induced ferroptosis (P < 0.05). And in the salvage experiment, the research team found that microrna-587 mimics inhibited PGM5-AS1-wild sequence fluorescence activity. The biological behavior of A549 after increasing (or silencing) PGM5-AS1 and microrna-587 was not different from that of cells transfected with microrna-587 negative control (P > 0.05). These results suggest that low-expressed PGM5-AS1 can promote lung cancer cell viability, inhibit apoptosis and resist ferroptosis through targeted increase of microrna-587.