Lnc-LINC00511 promotes gastric cancer progression by regulating MiR-29c-3p/TRIP13 axis through AKT/mTOR pathway.

Thyroid hormone receptor-interacting factor 13 (TRIP13) contributes to the development of several cancers, including hepatocellular carcinoma (HCC). Although these studies have found that TRIP13 is involved in other cancers, its specific function in gastric cancer requires further investigation. Therefore, this study aimed to investigate the hypothesis that LINC00511 may act as an oncogenic factor in gastric cancer by influencing and regulating the expression level of TRIP13. This relationship has the potential to reveal the molecular mechanisms driving gastric cancer progression and further elucidate the roles of LINC00511 and TRIP13 in gastric cancer. In this study, we confirmed that LINC00511 could act as a ceRNA targeting miR-29c-3p to further regulate the expression of TRIP13. LINC00511 was also found to be able to be positively regulated by the transcription factor IRF9. In addition, TRIP13 could activate the AKT/mTOR pathway by interacting with its downstream protein ACTN2, thus promoting the proliferation of GC cells. lnc-LINC00511 could promote GC progression by regulating the miR-29c-3p/TRIP13 axis and activating the AKT/mTOR pathway.