HIF-1α contributes to metastasis in choriocarcinoma by regulating DEC1 expression
Clin. transl. oncol. (Print)
; 25(6): 1641-1649, jun. 2023. ilus
Article
in En
| IBECS
| ID: ibc-221196
Responsible library:
ES1.1
Localization: ES15.1 - BNCS
ABSTRACT
Purpose To elucidate the underlying mechanism of HIF-1α in migration and invasion of choriocarcinoma. Methods Cell proliferation was determined by CCK-8 assay when cell invasion was detected by transwell assay. The protein expression was detected by western blotting, immunohistochemistry, and qPCR assay. Result HIF-1α was shown to be strongly expressed in both clinical tumour tissues and cell lines in choriocarcinoma. When HIF-1α was efficiently knocked down in JEG3 cells, the proliferation rate was reduced by approximately 50% and the number of cells that migrated through the transwell insert was greatly decreased. The cell invasion rate was also significantly reduced. Moreover, typical markers of epithelialmesenchymal transition such as E-cadherin, were increased, while vimentin and αSMA were decreased after HIF-1α knockdown. In contrast, overexpression of DEC1 reversed the effects of HIF-1α knockdown. Cell proliferation, migration, and invasion were partially recovered. The level of E-cadherin was decreased, while the level of vimentin and αSMA was increased. In addition, the level of β-catenin and LEF1 was downregulated after HIF-1α knockdown. The expression of MMP2 and MMP9 also declined. However, overexpression of DEC1 after HIF-1α knockdown partially reversed the expression pattern of these molecules. Conclusion HIF-1α contributed to EMT and metastasis through activation of canonical β-catenin signalling in choriocarcinoma and this process was dependent on DEC1. This study provides a new mechanism of HIF-1α in choriocarcinoma and suggests that intervention with DEC1 might be a promising therapeutic choice for choriocarcinoma (AU)
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Collection:
06-national
/
ES
Database:
IBECS
Main subject:
Choriocarcinoma
/
Beta Catenin
Limits:
Female
/
Humans
Language:
En
Journal:
Clin. transl. oncol. (Print)
Year:
2023
Document type:
Article