Sie befinden Sich nicht im Netzwerk der Universität Paderborn. Der Zugriff auf elektronische Ressourcen ist gegebenenfalls nur via VPN oder Shibboleth (DFN-AAI) möglich. mehr Informationen...
CENPK orchestrates ovarian cancer progression via GOLPH3-Mediated activation of mTOR signaling
Ist Teil von
Molecular and cellular endocrinology, 2024-08, Vol.589, p.112253, Article 112253
Ort / Verlag
Ireland: Elsevier B.V
Erscheinungsjahr
2024
Link zum Volltext
Quelle
Elsevier ScienceDirect Journals
Beschreibungen/Notizen
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.