PSMG3-AS1 (PSMG3 Antisense RNA 1)

The accumulating evidence suggests that PSMG3-AS1 may serve as both a prognostic biomarker and a potential therapeutic target. However, further research is necessary to fully understand the molecular mechanisms by which PSMG3-AS1 influences cancer biology and to explore its clinical implications in cancer diagnosis and treatment.

Significantly, the proliferative and invasive capabilities of MKN-45 and AGS cells were notably reduced following transfection with PSMG3-AS1 siRNA. The results of our study indicate that disruption of the LncRNA PSMG3-AS1 gene may impact the CAV1/miR-451a signaling pathway, thereby leading to a reduction in the ability of gastric cancer cells to multiply and invade.

RGN expression was closely associated with prognosis of LUSC patients and played an important role in tumor microenvironment. This suggests that RGN could be a promising biomarker for assessing immunotherapy efficacy and prognosis.

Cell proliferation analysis showed that PSMG3-AS1 reduced the inhibitory effects of miR-106b overexpression on cell proliferation. Taken together, our data suggested that PSMG3-AS1 could downregulate miR-106b through DNA methylation to suppress PC cell proliferation.

PSMG3-AS1 increased OSCC cell proliferation and tumor growth and suppressed the inhibitory role of miR-141 in cell proliferation and tumor growth. Therefore, PSMG3-AS1 may inhibit the maturation of miR-141 to promote OSCC cell proliferation.

Mechanistically, PSMG3-AS1 directly binds to c-Myc and thus stabilizes c-Myc in the nucleus to promote the survival of GBM cells under treatment of TMZ. Our data demonstrated an unreported role of PSMG3-AS1 in TMZ resistance and provide a potential novel target to tackle TMZ resistance in GBM.