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Effects of Estrogen and Estrogen Receptors on Glucose Metabolism of Liver Cancer Cell


Affiliations
1 Structural Biology Miami University, Oxford, Ohio, United States
2 Department of Biology, Miami University Oxford, Ohio, United States
 

Epidemiology data show that men have a much higher incidence of hepatocellular carcinoma (HCC) than women, suggesting that estrogen and its receptors may inhibit HCC development and progression. To investigate the potential inhibitory mechanisms of estrogens on HCC development, human cancer cell line HepG2 was treated with different concentrations of estrogen and specific agonists for estrogen receptor (ER) ERα and ERβ to determine the roles of estrogen and its receptors in HepG2 cancer cell proliferation, apoptosis, gene expression, and metabolic pathways. Our findings indicated that estrogen and its receptors suppressed HepG2 cell growth by inhibiting cell proliferation and stimulating cell apoptosis via primary activation of ERβ, and by affecting HepG2 glucose metabolism via primary activation of ERα. Identifying roles of different estrogen receptors would provide comprehensive understanding of estrogenic mechanisms in HCC development and shed light on potential treatments for HCC patients.

Keywords

HepG2, Estradiol, ERα, ERβ, Glycolysis, Oxidative Phosphorylation.
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  • Effects of Estrogen and Estrogen Receptors on Glucose Metabolism of Liver Cancer Cell

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Authors

Minqian Shen
Structural Biology Miami University, Oxford, Ohio, United States
Haifei Shi
Department of Biology, Miami University Oxford, Ohio, United States

Abstract


Epidemiology data show that men have a much higher incidence of hepatocellular carcinoma (HCC) than women, suggesting that estrogen and its receptors may inhibit HCC development and progression. To investigate the potential inhibitory mechanisms of estrogens on HCC development, human cancer cell line HepG2 was treated with different concentrations of estrogen and specific agonists for estrogen receptor (ER) ERα and ERβ to determine the roles of estrogen and its receptors in HepG2 cancer cell proliferation, apoptosis, gene expression, and metabolic pathways. Our findings indicated that estrogen and its receptors suppressed HepG2 cell growth by inhibiting cell proliferation and stimulating cell apoptosis via primary activation of ERβ, and by affecting HepG2 glucose metabolism via primary activation of ERα. Identifying roles of different estrogen receptors would provide comprehensive understanding of estrogenic mechanisms in HCC development and shed light on potential treatments for HCC patients.

Keywords


HepG2, Estradiol, ERα, ERβ, Glycolysis, Oxidative Phosphorylation.

References