akt inhibitor viii  (MedChemExpress)

Journal: Frontiers in Oncology

Article Title: Hypoxia induced DNMT3B and SHP2 signaling promoted HCC via suppressing P53 and MYH11 protein expression

doi: 10.3389/fonc.2026.1794481

Figure Lengend Snippet: Regulation of hepatocellular carcinoma progression by CBFβ-MYH11 under hypoxic conditions through AKT and SHP2 pathways. (A) Western blot experiments were performed to detect p-AKT, p-SHP2, p-DNMT3B, P53 and MYH11 protein banding plots and relative protein expression statistics in Normoxic group, Hypoxic group, Normoxic+MK-2206 group, Hypoxic+MK-2206 group, Normoxic+Batoprotafib group and Hypoxic+Batoprotafib group; (B) Methylation-qPCR assay was performed to detect the methylation levels of P53 and MYH11 in Normoxic group, Hypoxic group, Normoxic+MK-2206 group, Hypoxic+MK-2206 group, Normoxic+Batoprotafib group and Hypoxic+Batoprotafib group; (C) RT-qPCR experiments were performed to detect the relative mRNA expression of P53β and Δ133P53 in Normoxic group, Hypoxic group, Normoxic+MK-2206 group, Hypoxic+MK-2206 group, Normoxic+Batoprotafib group and Hypoxic+Batoprotafib group Statistical plots of the amount of P53β and Δ133P53. Data were expressed as mean ± standard deviation. N = 3; *P<0.05; **P<0.01; ns P>0.05: There was no significant difference.

Article Snippet: Akt inhibitor MK-2206 (5 nM), SHP2 inhibitor Batoprotafib (0.005 μM), P53 inhibitor Pifithrin-α (10 μM), and P53 activator Tenovin-1 (10 μM) were purchased from MCE.

Techniques: Western Blot, Expressing, Methylation, Quantitative RT-PCR, Standard Deviation

Journal: Frontiers in Oncology

Article Title: Hypoxia induced DNMT3B and SHP2 signaling promoted HCC via suppressing P53 and MYH11 protein expression

doi: 10.3389/fonc.2026.1794481

Figure Lengend Snippet: Migration, invasion, and angiogenesis of hepatocellular carcinoma under hypoxia induced by CBFβ-MYH11 through AKT and SHP2 pathways. (A) Western blot experiments were performed to detect the strip maps of MMP2 and HIF1α in the Normoxic group, Hypoxic group, Normoxic+MK-2206 group, Hypoxic+MK-2206 group, Normoxic+Batoprotafib group, and Hypoxic+Batoprotafib group and the relative protein expression statistics; GAPDH as control protein; N = 3; (B) Graphs of experimental results of Transwell assay to detect the cell migration ability of Normoxic group, Hypoxic group, Normoxic+MK-2206 group, Hypoxic+MK-2206 group, Normoxic+Batoprotafib group, and Hypoxic+Batoprotafib group as well as statistical graphs of the number of migrated cells; N = 3; (C) Plots of experimental results of cell scratch assay to detect cell migration ability of Normoxic group, Hypoxic group, Normoxic+MK-2206 group, Hypoxic+MK-2206 group, Normoxic+Batoprotafib group, and Hypoxic+Batoprotafib group as well as statistical plots of cell spacing; N = 3; (D) Graphs of the experimental results of Angiogenesis experiment to detect the angiogenic ability of Normoxic group, Hypoxic group, Normoxic+MK-2206 group, Hypoxic+MK-2206 group, Normoxic+Batoprotafib group, and Hypoxic+Batoprotafib group, as well as statistical graphs of the number of blood vessels; N = 3; (E) The results of HE staining experiments were plotted as well as the statistics of the number of blood vessels. N = 8; Data were expressed as mean ± standard deviation. **P<0.01; ns P>0.05: There was no significant difference.

Article Snippet: Akt inhibitor MK-2206 (5 nM), SHP2 inhibitor Batoprotafib (0.005 μM), P53 inhibitor Pifithrin-α (10 μM), and P53 activator Tenovin-1 (10 μM) were purchased from MCE.

Techniques: Migration, Western Blot, Stripping Membranes, Expressing, Control, Transwell Assay, Wound Healing Assay, Staining, Standard Deviation