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Estrogen and ER[alpha] enhanced [beta]-catenin degradation and suppressed its downstream target genes to block the metastatic function of HA22T hepatocellular carcinoma cells via modulating GSK-3[beta] and [beta]-TrCP expression
In our previous experiments, we found [beta]-catenin was highly expressed in the tumor area with high invasive ability and poor prognosis. In this study, we have examined the mechanism by which ER[alpha] regulates [beta]-catenin expression as well as the metastasis ability of hepatocellular cancer HA22T cells. To identify whether the anticancer effect of estrogen and ER[alpha] is mediated through suppression of [beta]-catenin expression, we co-transfected pCMV-[beta]-catenin and ER[alpha] into HA22T cells, and determined the cell motility by wound healing, invasion, and migration assays. Results showed that estrogen and/or ER[alpha] inhibited [beta]-catenin gene expression and repressed HA22T cell motility demonstrated that similar data was observed in cells expressing the ER[alpha] stable clone. Moreover, we examined the protein-protein interaction between ER[alpha] and [beta]-catenin by immunostain, co-immunoprecipitation, and Western blotting. E2 enhanced the binding of ER[alpha] with [beta]-catenin and then triggered [beta]-catenin to bind with E3 ligase ([beta]TrCP) to promote [beta]-catenin degradation. Finally by employing systematic ChIP studies, we showed ER[alpha] can interact directly with the [beta]-catenin promoter region following E2 treatment. All our results reveal that estrogen and ER[alpha] blocked metastatic function of HA22T cells by modulating GSK3[beta] and [beta]TrCP expression and further enhanced [beta]-catenin degradation and suppressed its downstream target genes. © 2016 Wiley Periodicals, Inc. Environ Toxicol 32: 519-529, 2017.
Estrogen and ER[alpha] enhanced [beta]-catenin degradation and suppressed its downstream target genes to block the metastatic function of HA22T hepatocellular carcinoma cells via modulating GSK-3[beta] and [beta]-TrCP expression
In our previous experiments, we found [beta]-catenin was highly expressed in the tumor area with high invasive ability and poor prognosis. In this study, we have examined the mechanism by which ER[alpha] regulates [beta]-catenin expression as well as the metastasis ability of hepatocellular cancer HA22T cells. To identify whether the anticancer effect of estrogen and ER[alpha] is mediated through suppression of [beta]-catenin expression, we co-transfected pCMV-[beta]-catenin and ER[alpha] into HA22T cells, and determined the cell motility by wound healing, invasion, and migration assays. Results showed that estrogen and/or ER[alpha] inhibited [beta]-catenin gene expression and repressed HA22T cell motility demonstrated that similar data was observed in cells expressing the ER[alpha] stable clone. Moreover, we examined the protein-protein interaction between ER[alpha] and [beta]-catenin by immunostain, co-immunoprecipitation, and Western blotting. E2 enhanced the binding of ER[alpha] with [beta]-catenin and then triggered [beta]-catenin to bind with E3 ligase ([beta]TrCP) to promote [beta]-catenin degradation. Finally by employing systematic ChIP studies, we showed ER[alpha] can interact directly with the [beta]-catenin promoter region following E2 treatment. All our results reveal that estrogen and ER[alpha] blocked metastatic function of HA22T cells by modulating GSK3[beta] and [beta]TrCP expression and further enhanced [beta]-catenin degradation and suppressed its downstream target genes. © 2016 Wiley Periodicals, Inc. Environ Toxicol 32: 519-529, 2017.
Estrogen and ER[alpha] enhanced [beta]-catenin degradation and suppressed its downstream target genes to block the metastatic function of HA22T hepatocellular carcinoma cells via modulating GSK-3[beta] and [beta]-TrCP expression
2017
Article (Journal)
English
| British Library Online Contents | 2005