PT  - JOURNAL ARTICLE
AU  - YEN-JU LEE
AU  - JING-GUNG CHUNG
AU  - ZHAO-LIN TAN
AU  - FEI-TING HSU
AU  - YU-CHANG LIU
AU  - SONG-SHEI LIN
TI  - ERK/AKT Inactivation and Apoptosis Induction Associate With Quetiapine-inhibited Cell Survival and Invasion in Hepatocellular Carcinoma Cells
AID  - 10.21873/invivo.12054
DP  - 2020 Sep 01
TA  - In Vivo
PG  - 2407--2417
VI  - 34
IP  - 5
4099  - http://iv.iiarjournals.org/content/34/5/2407.short
4100  - http://iv.iiarjournals.org/content/34/5/2407.full
SO  - In Vivo2020 Sep 01; 34
AB  - Background/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 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. 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.