Journal: Cancer Biology & Medicine
Article Title: HBx-mediated GPT2 suppression promotes liver cancer development by downregulating ADH1A
doi: 10.20892/j.issn.2095-3941.2025.0236
Figure Lengend Snippet: Influence of GPT2 on mTOR signaling pathway activation and regulation of ADH1A expression. (A) Effects of inhibition of mTOR with AZD8055 on ADH1A expression in LC cells. (B) Effects of activation of mTOR with MHY1485 on ADH1A expression in LC cells. (C) Effects of GPT2 on mTOR activation and ADH1A expression in LC cells. (D) Effects of AKT activation mediated by the activator SC79 on mTOR sensitization and ADH1A expression in LC cells. (E) Effects of GPT2 on the activation of AKT and mTOR in LC cells. (F) Effects of GPT2 on mTOR activation and ADH1A expression mediated by AKT activation in LC cells. (G) AKT–mTOR interaction, assessed with co-IP assays. (H) Effects of GPT2 on AKT–mTOR interaction, measured with co-IP assays in LC cells. ADH1A, alcohol dehydrogenase 1A; AKT, protein kinase B; co-IP, co-immunoprecipitation; GPT2, glutamic-pyruvic transaminase 2; LC, liver cancer; mTOR, mammalian target of rapamycin.
Article Snippet: The AKT activator SC79, the mTOR pathway activator MHY1485, and its inhibitor AZD8055 were obtained from MedChemExpress (Shanghai, China).
Techniques: Activation Assay, Expressing, Inhibition, Co-Immunoprecipitation Assay, Immunoprecipitation