ERK/AKT Inactivation and Apoptosis Induction Associate With Quetiapine-inhibited Cell Survival and Invasion in Hepatocellular Carcinoma Cells

ERK/AKT 失活和凋亡诱导与喹硫平抑制肝细胞癌细胞存活和侵袭有关

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作者:Yen-Ju Lee, Jing-Gung Chung, Zhao-Lin Tan, Fei-Ting Hsu, Yu-Chang Liu #, Song-Shei Lin #

Aim

Quetiapine, an atypical antipsychotic, has been encountered as a potential protective agent to suppress various types of tumor growth. However, the inhibitory mechanism of quetiapine in hepatocellular carcinoma (HCC) still remains unclear. The purpose of present study was to investigate the inhibitory mechanism of quetiapine on cell survival and invasion in HCC. Materials and

Conclusion

The apoptosis induction, the decreased expression of ERK/AKT-mediated anti-apoptotic and the metastasis-associated proteins were associated with quetiapine-inhibited cell survival and invasion in HCC in vitro.

Methods

Changes of apoptotic signaling, migration/invasion ability, and signaling transduction involved in cell survival and invasion were evaluated with flow cytometry, migration/invasion, and western blot assays.

Results

Quetiapine inhibited cell proliferation and migration/invasion in SK-Hep1 and Hep3B cells. Quetiapine induced extrinsic and intrinsic apoptotic pathways. Activation of extracellular signal-regulated kinases (ERK), protein kinase B (AKT), nuclear factor kappa-light-chain-enhancer of activated B cells (NF-ĸB), expression of anti-apoptotic, and metastasis-associated proteins were decreased by quetiapine.

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