ArticleHeliyon2024
Estrogen regulates PDPK1 to promote cell proliferation in epithelial ovarian cancer.
Article in Heliyon, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
What it found
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Who cites it
3 citing papers in PubMed.
- Plant Metabolites Screening Identifies 7-epi-10-Deacetyltaxol Inhibiting Cell Division by Interfering With the Cell Cycle and Microtubule Organization.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Phosphoinositide-dependent kinase 1 (PDK1) in cancer: molecular insights and therapeutic strategies.Frontiers in chemistry · 2026Review
- Global, regional, and national burden of ovarian cancer due to high BMI, 1990-2021 and projections to 2050: a systematic analysis based on the global burden of disease 2021 study.Frontiers in nutrition · 2026Article
Corrections and comments
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Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Epithelial ovarian cancer (EOC) is a common estrogen-sensitive tumor that poses a serious threat to women 's health, and the mortality rate of EOC ranks first among malignant tumors in females. Studies have indicated a strong link between estrogen abnormality and EOC progression. We accidently found that 3-phosphoinositide-dependent protein kinase-1 (PDPK1) is highly expressed in EOC tissues. Further, estrogen also up-regulates the expression of PDPK1 in EOC cells. Notably, the expression of PDPK1 is controlled strictly, and its expression can determine the fate of cells. However, to date, the molecular mechanism by which estrogen elicits PDPK1 expression in EOC cells, and the role of PDPK1 in estrogen-driven EOC cells are not well defined. In this research, we found that a high expression of PDPK1 was associated with poor prognosis in patients with ovarian cancer. Further, estrogen stimulated the increase of PDPK1 protein expression through estrogen receptor ESR1. The depletion or overexpression of PDPK1 affected the inhibition or amplification of estrogen-driven EOC cell proliferation, and the knockdown of PDPK1 suppressed the migration of EOC cells by estrogen while promoting cell apoptosis. This suggests a critical functional association between estrogen and PDPK1 in the process of EOC. The expression of messenger RNA for cyclin A1, cyclin-dependent kinase 2 (CDK2), matrix metallopeptidase 2 (MMP2), and bcl-2 associated x protein (Bax) is regulated by PDPK1 under estrogen treatment. Our results indicated that PDPK1 plays a role as an oncogene in the development of EOC; hence, elucidating the mechanism by which estrogen promotes EOC progression by regulating PDPK1 expression.
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Registered trials
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