CENPA (Centromere protein A)

We found that silencing CENPA significantly increased reactive oxygen species production and mitochondrial membrane potential abnormalities leading to inhibition of cell viability and proliferation and cell death, suggesting that CENPA is closely associated with the development of KIRC. In conclusion, IGF2BP3 and its downstream CENPA signature can be used for prognostic prediction of KIRC.

This study is the first to establish a CENP-based prognostic model for BC, offering novel biomarkers and potential therapeutic targets for personalized treatment. Additionally, the biological function of the key molecule MMP1 was validated through both in vitro and in vivo experiments.

This study demonstrates that unsupervised clustering combined with WGCNA and ML enables the discovery of clinically relevant molecular signatures in PCa. Our findings establish TPX2-centered networks together with biological pathways implicated in mitotic regulation and DNA damage repair as key drivers of tumor evolution, providing a biologically informed source for biomarker development, drug testing and mechanistic studies.

Additionally, we explore the potential of targeting these molecules to enhance the efficacy of radiation therapy and improve patient outcomes. Our study contributes to the comprehension of the molecular processes underlying oral cancer and provides insights into the development of novel therapeutic strategies based on personalized medicine.

Overall, from this report and earlier studies on HJURP, we conclude that DDR functions of CENP-A chaperones are conserved across eukaryotes. The revelation that these chaperones promote genome stability in more than one pathway has clinical significance.

Glioblastoma (GBM) is a highly aggressive and therapeutically challenging brain tumor characterized by poor prognosis, rapid recurrence, and resistance to standard treatments such as temozolomide (TMZ)...Disruption of CPC function led to reduced mitotic activity and increased mitotic defects in treated cultures. Collectively, these findings indicate that dual inhibition of CDC25 and HDAC by MPT1B394 disrupts CPC-mediated mitosis and aberrant cell cycle progression, representing a promising therapeutic avenue for GBM treatment.

We finally observed reduced physiological DNA recombination and somatic hypermutation but increased genomic instability in DIS3-deficient cells, in agreement with the higher levels of IGH translocations observed in our large cohort of DIS3-mutant MM patients. Together, these results underscore the essential role of DIS3 in regulating B cell proliferation, DNA recombination, and physiological or malignant PC differentiation in humans.

This study investigates differentially expressed genes and pathways in hepatoblastoma, shedding light on disease mechanisms and identifying potential biomarkers for diagnosis and treatment. The findings highlight therapeutic strategies involving Wnt inhibition, ferroptosis induction, and cell cycle regulation, guiding future research into innovative treatment modalities for hepatoblastoma. Key genes CENPA, HMGA2, WIF1, DKK1, and SLC7A11 warrant further investigation due to their potential implications in hepatoblastoma tumorigenesis and proliferation. This study expands the current understanding of genetic influences of hepatoblastoma and informs future research into drivers of hepatoblastoma pathogenesis by leveraging a novel approach utilizing publicly available data.

This signature consisted of BUB1, BUB1B, CDK1, CENPA, CKAP2L, IQGAP3, MKI67, NDC80, PBK, RRM2, TOP2A, and TTK. Our analysis provides a basis for the development of a novel prognostic test to predict the survival time of patients.

Importantly, EP400K1085G cells exhibit CIN phenotypes in stable, near-diploid RPE1 cells with wild-type p53. In summary, our findings expand the role of EP400 from nucleosome destabilization for histone exchange to preventing the stable association of CENP-A with non-centromeric regions and CIN.

Therefore, discovering the underlying pathways and mechanisms responsible for the formation, regulation and maintenance of the centromere is important to our understanding of genome stability, epigenetic inheritance, and in providing the knowledge to help generate possible treatments and therapeutics. Here, we review various molecular pathways and mechanisms implicated in maintaining centromere identity and highlight some of the key outstanding questions with a focus on the human centromere.

HJURP is a key regulator in cancer biology with diagnostic and therapeutic potential. Targeting HJURP may provide novel strategies for personalized cancer treatment and improved patient outcomes.