Fig 1: NAC reduced the cytotoxicity of TEOA and inhibited autophagy by restoring mTOR/p70S6k signaling pathway in SW1990 cells. (A) SW1990 cells were treated with TEOA alone or in combination with 0.5 mM NAC, and then ROS levels were measured by flow cytometry after 8 h. (B) Statistical analysis of relative ROS level and the results were presented as the mean ± SD from three independent experiments. (C) SW1990 cells were treated with TEOA alone or in combination with 0.5 mM NAC. After 12 h, images were captured using optical microscope (20×). (D) SW1990 cells were treated with TEOA at various concentrations alone or in combination with 0.5 mM NAC for 12 h and cell viability was detected by CCK-8 assay. (E) After incubating with individual TEOA or combination with NAC for 8 h, protein expression of mTOR / p70s6k signaling pathway was determined by western blot (?p < 0.05; ??p < 0.01; ???p < 0.001, versus control).
Fig 2: TEOA induced autophagy via inhibiting mTOR/p70s6k/S6 signaling pathway in pancreatic cancer cells. (A,B) After exposure to TEOA for 8 h, SW1990 and PANC1 cells were collected to measure the signaling pathway of mTOR/p70s6k/S6, GAPDH used as a loading control. (C–E) Relative quantitative analysis of SW1990 was shown. (F–H) Relative quantitative analysis of PANC1 was shown (?p < 0.05; ??p < 0.01; ???p < 0.001, versus control).
Fig 3: Overexpression of HIP1R or inhibition of miR-92a-3p modulates the malignancy of PAAD cells by targeting PI3K/Akt pathway. (A) GSEA analysis revealed a negative correlation between HIP1R expression and the gene expressions in PI3K/Akt pathway. (B) The phosphorylation levels of Akt, mTOR, S6K and S6 were examined by Western blot in PAAD cells with different treatments (NC group, pcDNA3.1-HIP1R group, miR-92a-3p mimic group, miR-92a-3p mimic + pcDNA3.1-HIP1R group). (C) Cell proliferation abilities in different groups (NC group, miR-92a-3p mimic group, miR-92a-3p mimic + Rigosertib (a PI3K/AKT inhibitor)) were investigated by CCK8 assay. (D) The apoptotic events in cells with different treatments (NC group, miR-92a-3p mimic group, miR-92a-3p mimic + Rigosertib) were quantified by flow cytometry. (E) The relative level of p-Akt in the xenograft tissues was measured by IHC staining. *p < 0.05, **p < 0.01, ***p < 0.001
Supplier Page from Abcam for Anti-S6K1 (phospho S424) antibody