Proscillaridin A inhibits hepatocellular carcinoma progression through inducing mitochondrial damage and autophagy.

Acta Biochim Biophys Sin (Shanghai)

Key Laboratory of Medical Molecular Virology (NHC & MOE & CAMS), Institutes of Biomedical Sciences, Department of Medical Microbiology and Parasitology, School of Basic Medical Sciences,Shanghai Medical College, Fudan University, Shanghai 200032, China.

Published: January 2021

AI Article Synopsis

  • Hepatocellular carcinoma (HCC) is a major global health issue with limited treatment options, necessitating new drug development.
  • Proscillaridin A (ProA), a cardiac glycoside, showed significant anticancer effects on various HCC cell lines, inhibiting their growth and spread.
  • The mechanisms behind ProA's effectiveness include inducing cell apoptosis and autophagy, highlighting its potential as a therapeutic agent for HCC treatment.

Article Abstract

Hepatocellular carcinoma (HCC) is one of the leading causes of cancer-related deaths globally. At present, drug options for systemic treatment of HCC are very limited. There is an urgent need to develop additional effective drugs for HCC treatment. In the present study, we found that proscillaridin A (ProA), a cardiac glycoside, exerted a strong anticancer effect on multiple HCC cell lines. ProA significantly inhibited the cell proliferation, migration, and invasion of HCC cells. ProA also had a marked inhibitory effect on the progression of HCC in the MHCC97H xenograft nude mouse model. ProA-mediated suppression of HCC was closely related to cell apoptosis. ProA-treated HCC cells displayed significant mitochondrial damage and elevated reactive oxygen species production, resulting in profound cell apoptosis. Meanwhile, ProA also played a role in autophagy induction in HCC cells. Defects in autophagy partially relieved ProA's anticancer effect in HCC cells. Our findings demonstrate that ProA can effectively inhibit HCC progression and may serve as a potential therapeutic agent for HCC treatment.

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Source
http://dx.doi.org/10.1093/abbs/gmaa139DOI Listing

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