MK2206 inhibits hepatocellular carcinoma cellular proliferation via induction of apoptosis and cell cycle arrest

Abstract Background Hepatocellular carcinoma (HCC) is commonly diagnosed at an advanced stage and has limited effective treatment options. The aberrant regulation of the phosphoinositide 3-kinase/Akt pathway in HCC makes it an attractive therapeutic target. The effect of MK2206, a novel, allosteric Akt inhibitor, on HCC cells is not yet fully understood. We hypothesized that inhibition of Akt by MK2206 would impact cellular viability. Materials and methods Human Huh7, Hep3B, and HepG2 cell lines were treated with 0–2 μM of MK2206 for 96 h. Cell viability was determined by using 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay. Western blot analysis was used to examine the expression level of various protein markers to assess the mechanism of drug action and proliferation inhibition. Results 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay showed a reduction in cellular viability by ≥55% for all cell lines (control versus 2 μM MK2206; P