Knockdown of anti-silencing function 1B histone chaperone induces cell apoptosis via repressing PI3K/Akt pathway in prostate cancer

作者: Guangye Han , Xinjun Zhang , Pei Liu , Quanfeng Yu , Zeyu Li

DOI: 10.3892/IJO.2018.4526

关键词: LNCaPKinaseAkt/PKB signaling pathwayBiologyCell cycle checkpointProtein kinase BPI3K/AKT/mTOR pathwayCell cycleCancer researchViability assay

摘要: Prostate cancer (PCa) is one of the most common malignancies among males worldwide. Anti-silencing function 1B histone chaperone (ASF1B) has been reported to be involved in PCa. The present study aimed investigate role and molecular mechanism ASF1B Data genes were obtained from Cancer Genome Atlas data- base. core gene was identified using DAVID website. Cell viability colony formation detected a cell counting kit-8 assay crystal violet staining, respectively. cycle distribution apoptosis assessed flow cytometry analysis. corresponding factors analyzed by reverse transcription-quantitative polymerase chain reaction western blotting. It demonstrated that highly expressed PCa tissues cells compared with non-PCa cells, While siRNA-ASF1B significantly reduced formation, it promoted apoptosis, G1 phase arrest LNCap as well C4-2 cells. revealed reduce level B-cell lymphoma-2 cyclin D1, enhance expression levels p53, caspase-3 Bcl-2 associated X protein. Furthermore, phosphorylation phosphatidylinositol 3 kinase (PI3K) protein B (Akt) decreased group mock group. In summary, silencing suppressed proliferation, Inhibition PI3K/Akt signaling pathway pertinent si-ASF1B. This phenomenon suggests downregulation may aid inhibiting progression

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