Differential regulation of AKT1 contributes to survival and proliferation in hepatocellular carcinoma cells by mediating Notch1 expression

The RAC serine/threonine-protein kinase (AKT) family of serine/threonine protein kinases, particularly the AKT1 isoform, has been identified abnormally expressed in hepatocellular carcinoma (HCC) cells, and is highly associated with cell behavior, including proliferation, survival, metabolism, and tumorigenesis. However, the specific mechanism by which AKT1 elicits these effects requires further study. The purpose of the present study was to reveal the effects of AKT1 on the survival and proliferation of HCC cells, and to investigate the mechanisms involved. Western blotting and reverse transcription-quantitative polymerase chain reaction (RT-qPCR) to evaluate the expression levels of AKT1 in HCC SMMC-7721 cell line. Molecular mechanisms and the influences of different regulation the expression of AKT1 on HCC cell growth, proliferation were determined by western blotting, MTT and colony formation assays, cell cycle and apoptosis were investigated by flow cytometry. The activation of AKT1 suppressed the expression of phosphatase and tensin homolog and increased the activation of Notch1. The inhibition of AKT1 effectively suppressed the expression of Notch1. Furthermore, the data of the present study indicated that B-cell lymphoma 2 and cyclin D1 is involved in the regulation of AKT1 expression.