Journal
FRONTIERS IN PHARMACOLOGY
Volume 12, Issue -, Pages -Publisher
FRONTIERS MEDIA SA
DOI: 10.3389/fphar.2021.607379
Keywords
17β -estradiol; hepatocellular carcinoma; oxidative stress; apoptosis; foxo3a phosphorylation
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Funding
- Guangzhou Health Care Co-innovation Major Plan Fund [201803040014]
- Innovation and Entrepreneurship Training Program of Guangdong Pharmaceutical University [202010573014]
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17 beta-estradiol can induce oxidative stress and apoptosis in HepG2 cells, potentially serving as a new treatment for hepatocellular carcinoma.
Liver cancer is associated with high mortality, particularly in patients infected with the hepatitis B virus. Treatment methods remain very limited. Here, we explored the effects of 17 beta-estradiol (E2) on apoptosis of various liver cell lines (LO2, HepG2, and HepG2.2.15 cells). Within a certain concentration range, 17 beta-estradiol induced oxidative stress and apoptosis of HepG2 cells, downregulated ER alpha-36 expression, and increased Akt and Foxo3a phosphorylation. p-Foxo3a became localized around the nucleus but did not enter the organelle. The levels of mRNAs encoding manganese superoxide dismutase (MnSOD) and catalase, to the promoters of which Foxo3a binds to trigger gene expression, were significantly reduced in HepG2 cells. 17 beta-estradiol had no obvious effects on LO2 or HepG2.2.15 cells. We speculate that 17 beta-estradiol may induce oxidative stress in HepG2 cells by increasing Foxo3a phosphorylation, thus promoting apoptosis. This may serve as a new treatment for hepatocellular carcinoma.
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