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Baicalein and Ly294002 induces liver cancer cells apoptosis via regulating phosphatidyl inositol 3-kinase/Akt signaling pathway


1 Department of Hepatobiliary Surgery, Affiliated Hospital of Southwest Medical University, Sichuan, P.R. China
2 Department of Obstetrics and Gynecology, The Affiliated TCM Hospital of Southwest Medical University, Sichuan, P.R. China
3 Experimental Medicine Center, The Affiliated Hospital of Southwest Medical University, Sichuan, P.R. China
4 Cancer Research Center of Southwest Medical University, Luzhou, Sichuan, P.R. China

Correspondence Address:
Jiyi Xia,
Cancer Research Center of Southwest Medical University, Luzhou, Sichuan
P.R. China
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Source of Support: None, Conflict of Interest: None

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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