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[Calenduloside E inhibits hepatocellular carcinoma cell proliferation and migration by down-regulating GPX4 and
Objective:
To investigate the molecular mechanism through which calenduloside E inhibits hepatocellular carcinoma (HCC) cell proliferation and migration.
Methods:
HCC cell lines HepG2 and Huh7 treated with calenduloside E were examined for changes in cell viability using CCK-8 assay and expressions of GPX4, SLC7A11, LC3, P62 and phosphorylation of Akt/mTOR using Western blotting. The effects LY294002 and Rapamycin (the inhibitor and activator of autophagy, respectively) on proliferation and migration of calenduloside E-treated HCC cells were evaluated using EdU and Transwell assays. The TCGA database was used to explore the expression levels of GPX4 and SLC7A11 in HCC and normal liver tissues and their correlation with the patients'survival outcomes. GPX4 and SLC7A11 expressions were also detected in HCC cells and normal hepatocytes using RT-qPCR and Western blotting.
Results:
Calenduloside E obviously inhibited the viability of HCC cells. GPX4 and SLC7A11 were highly expressed in HCC tissues and cell lines, and their expression levels were negatively correlated with the patients'survival. In HCC cell lines, calenduloside E significantly inhibited the expressions of GPX4 and SLC7A11 proteins, activated the Akt-mTOR pathway, and enhanced the expression of LC3 Ⅱ. The inhibitory effect of calenduloside E on GPX4 and SLC7A11 expressions was significantly enhanced by rapamycin but attenuated by LY294002. Inhibiting the autophagy pathway obviously diminished the inhibitory effect of calenduloside E on proliferation and migration of HCC cells, while activating this pathway produced the opposite effect.
Conclusion:
Calenduside E inhibits the proliferation and migration of HCC cells by down-regulating GPX4 and SLC7A11 expression via the autophagy pathway.
Insights
Calenduloside E inhibits hepatocellular carcinoma (HCC) cell growth and spread by reducing GPX4 and SLC7A11 levels through the autophagy pathway, offering a potential new therapeutic strategy.
Area of Science:
- Molecular Biology
- Oncology
- Biochemistry
Context:
- Hepatocellular carcinoma (HCC) is a significant global health concern with limited treatment options.
- Understanding the molecular mechanisms underlying HCC progression is crucial for developing targeted therapies.
Purpose:
- To elucidate the molecular mechanism by which calenduloside E inhibits HCC cell proliferation and migration.
- To investigate the role of GPX4, SLC7A11, and the autophagy pathway in calenduloside E's anti-cancer effects.
Summary:
- Calenduloside E demonstrated significant inhibition of HCC cell viability, proliferation, and migration.
- The compound down-regulated the expression of GPX4 and SLC7A11, proteins highly expressed in HCC and correlated with poor survival.
- These effects were mediated through the autophagy pathway, involving the Akt-mTOR signaling cascade.
Impact:
- This study reveals a novel mechanism of action for calenduloside E in HCC.
- The findings suggest calenduloside E as a potential therapeutic agent for HCC, targeting GPX4, SLC7A11, and autophagy.
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