CENPI (Centromere Protein I)

This study underscores the prognostic significance of CCCRGs in HCC and identifies CENPI as a key driver of tumor progression through the Hippo pathway. Furthermore, it reveals CENPI's role in promoting immune escape, suggesting novel therapeutic targets for HCC treatment.

Additional experiments demonstrated that the FOXM1/CENPI axis regulated the metabolism of Pro and Arg to promote GBM malignant progression modelled in vitro. In summary, our research indicated that FOXM1/CENPI signaling enhances the proliferation, migration, and invasion of GBM cells by promoting the metabolism of Arg and Pro.

CENPI is a critical oncogene in BCa, driving tumorigenesis and disease progression via the Wnt/β-catenin axis, which represents a promising biomarker and therapeutic target for BCa.

Sex-linked gene expression in lung tumours influences DDR and senescence pathways, correlating with survival outcomes. These findings highlight the importance of sex-specific analysis in lung cancer research and treatment.

Comparisons between two groups were analyzed using t-tests, and comparisons among multiple groups were analyzed using one-way ANOVA. The expression of CENPI and its correlation with clinical pathological features were analyzed using the

Mechanistically, Mechanistically, YTHDF3 interacted with Centromere protein I (CENPI) mRNAs to prolong stability of m6A-modified RNA. Our findings indicated that m6A reader YTHDF3 contributed to tumorigenesis and poor prognosis, providing a potential prognostic biomarker and therapeutic target for TNBC.

Our findings suggested that CCNB2, XRCC2, and CENPI may serve as key pathogenic mediators linking T2DM and BC. Targeting these molecules could potentially attenuate the adverse impacts of T2DM on BC progression.

We identified 4 reliable PCa biomarkers associated with pT staging that would be valuable for diagnosing and determining PCa prognosis.

What's more, the knock down of CENPI inhibited the expression of CDK2 in lung adenocarcinoma (LUAD), and resulted in the arrest of G0/G1 phase and apoptosis. Besides, CENPI was related to immune cells infiltration and drug sensitivity in pan-cancer, and can act as a potential treatment target to cure cancer patients.

Furthermore, drug sensitivity assay showed that vorinostat inhibit CENPI expression and ACC cell growth. Additionally, si-RNA mediated knockdown of CENPI inhibited ACC cell growth and invasion and showed synergistic anti-proliferation effect with AURKB inhibitor barasertib. Pan-cancer analysis demonstrated that CENPI is a potential diagnostic and prognostic biomarker in various cancers as well as an anti-ACC therapeutic target.