Protective Effect of Escitalopram on Hepatocellular Carcinoma by Inducing Autophagy

Background: Hepatocellular carcinoma (HCC) is an aggressive cancer with poor prognosis. Although recent research has indicated that selective serotonin reuptake inhibitors (SSRIs), including escitalopram, have anticancer effects, little is known about the effects of escitalopram on HCC. Methods: Bot...

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Published in:International journal of molecular sciences 2022-08, Vol.23 (16), p.9247
Main Authors: Chen, Li-Jeng, Hsu, Tsai-Ching, Chan, Hsiang-Lin, Lin, Chiao-Fan, Huang, Jing-Yu, Stewart, Robert, Tzang, Bor-Show, Chen, Vincent Chin-Hung
Format: Article
Language:English
Subjects:
Antidepressants
Apoptosis
Autophagy
Breast cancer
Cancer therapies
Cell proliferation
Citalopram
Cohort analysis
Drug dosages
escitalopram
Hepatocellular carcinoma
hepatocellular carcinoma (HCC)
In vitro methods and tests
In vivo methods and tests
Kinases
Laboratories
Liver cancer
Medical prognosis
nationwide population-based cohort study
Population studies
Population-based studies
Proteins
selective serotonin reuptake inhibitors (SSRIs)
Serotonin
Serotonin uptake inhibitors
Tumors
Xenografts
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Summary:Background: Hepatocellular carcinoma (HCC) is an aggressive cancer with poor prognosis. Although recent research has indicated that selective serotonin reuptake inhibitors (SSRIs), including escitalopram, have anticancer effects, little is known about the effects of escitalopram on HCC. Methods: Both in vitro and in vivo studies were conducted to verify the potentials of escitalopram on HCC treatment. To explore whether the effects of escitalopram are clinically consistent with laboratory findings, a nationwide population-based cohort study was also adopted to examine the association between escitalopram and HCC risk. Results: As compared with THLE-3 cells, escitalopram significantly inhibited the proliferation of HepG2 and Huh-7 cells. Specifically, escitalopram significantly induced autophagy in HepG2 and Huh-7 cells by increasing the LC3-II/LC3-I ratio and the expression of ATG-3, ATG-5, ATG-7, and Beclin-1 proteins. Moreover, escitalopram significantly inhibited the growth of xenografted Huh-7 cells in SCID mice that were treated with 12.5 mg/kg escitalopram. Accordingly, the risk of HCC was negatively correlated with escitalopram use. Conclusions: These findings provided evidence supporting the therapeutic potential of escitalopram for HCC. Both laboratory and nationwide population-based cohort evidence demonstrated the attenuated effects of escitalopram on HCC.
ISSN:1422-0067
1661-6596
1422-0067
DOI:10.3390/ijms23169247