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CENPK orchestrates ovarian cancer progression via GOLPH3-Mediated activation of mTOR signaling.
- Source :
-
Molecular & Cellular Endocrinology . Aug2024, Vol. 589, pN.PAG-N.PAG. 1p. - Publication Year :
- 2024
-
Abstract
- Ovarian cancer stands as a formidable clinical challenge, with limited therapeutic options. This investigation delves into the intricate molecular mechanisms governing ovarian cancer progression and uncovers Centromere Protein K (CENPK) as a central figure in disease pathogenesis. Elevated CENPK levels within ovarian cancer tissues conspicuously align with adverse clinical outcomes, positioning CENPK as a promising prognostic biomarker. Deeper exploration reveals a direct transcriptional connection between CENPK and the E2F1 transcription factor and clearly establishes E2F1's role as the master regulator of CENPK expression in ovarian cancer. Our inquiry revealing a suppression of tumor-promoting signaling pathways, most notably the mTOR pathway, upon CENPK silencing. Intriguingly, CENPK renders ovarian cancer cells more responsive to the mTOR inhibitor rapamycin, introducing a promising avenue for therapeutic intervention. In summation, our study unravels the multifaceted role of CENPK in ovarian cancer progression. It emerges as a prognostic indicator, a pivotal mediator of cell proliferation and tumorigenicity, and a regulator of the mTOR pathway, shedding light on potential therapeutic avenues for this formidable disease. • Elevated CENPK levels in ovarian cancer are associated with poor prognosis. • Direct transcriptional regulation between CENPK and E2F1. • CENPK regulates the mTOR signalling pathway. • Overexpression of CENPK makes ovarian cancer cells more sensitive to rapamycin. [ABSTRACT FROM AUTHOR]
Details
- Language :
- English
- ISSN :
- 03037207
- Volume :
- 589
- Database :
- Academic Search Index
- Journal :
- Molecular & Cellular Endocrinology
- Publication Type :
- Academic Journal
- Accession number :
- 177565619
- Full Text :
- https://doi.org/10.1016/j.mce.2024.112253