Journal of Cancer Research and Therapeutics · 2018 · 34 citations · 27 references
Life SciencesOncologyPharmacologyApoptosisCancer PharmacologyMolecular OncologyApoptosis In CancerApoptosis RegulationApoptotic SignalingCell Cycle SignalingCyclin-dependent KinasesOncogenic Signaling PathwaysCancer Cell ApoptosisCell Cycle InhibitionPhosphatidylinositol 3-Kinase Akt SignalingPhosphatidylinositol 3-Kinase PathwayPhosphatidylinositol 3-Kinase-akt SignalingPi3 Kinase-akt SignalingPi3k SignalingPi3k-akt Signaling Pathway
AIM: The aim of this study is to investigate the mechanism of baicalein in inducing human liver cell line SMMC-7721 apoptosis. MATERIALS AND METHODS: Twenty micromoles baicalein or 10 μM LY294002 was adopted to treat SMMC-7721 cells. Cell proliferation was tested by cell counting kit-8 assay. Cell cycle was determined by flow cytometry and cyclin D1 expression. Cell apoptosis was detected by annexin V/propidium iodide double staining. Phosphatidyl inositol 3-kinase (PI3K)/Akt signaling pathway was assessed by real-time polymerase chain reaction and Western blot. RESULTS: Baicalein suppressed liver cancer cell SMMC-7721 proliferation and induced cell apoptosis together with LY294002. Baicalein blocked cell cycle in G0-G1 phase and downregulated cyclin D1 level. Baicalein and LY294002 significantly suppressed PI3K/Akt signaling pathway-related molecule activity at both mRNA and protein levels (P < 0.05). CONCLUSION: Baicalein can inhibit liver cancer cell proliferation and promote cell apoptosis by affecting PI3K/Akt signaling pathway together with LY294002.
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