KIF23 (Kinesin Family Member 23)

Cisplatin treatment induces KIF23 expression in a concentration- and time-dependent manner. KIF23 recruits USP7, which removes the K48-linked ubiquitin chain of MYH9, thereby stabilising MYH9 and facilitating its nuclear transport. MYH9 recruits USP15, thereby stabilising MCM2, which, in turn, regulates the G1/S phase transition by binding to PCNA. Targeting the KIF23/MYH9/MCM2/PCNA axis sensitises cervical cancer cells to cisplatin.

Moreover, FBXW8 inhibited the overactivation of mitophagy and exerted tumor-suppressive effects by ubiquitinating and degrading NCBP2. This study reveals that NCBP2 regulates alternative splicing and mitophagy to influence cervical cancer progression, providing new potential therapeutic targets and strategies for cervical cancer treatment.

Previous study shows KIF23 takes part in raising Cell Proliferation in Hepatocellular carcinoma cells and AURKA shows notable overexpression in cancer tissues, which indicates that KIF23 and AURKA showed promising character to become possible biomarkers for OSCC. Further analysis needed to justify the statement.

UriPred efficiently predicts urinary proteins using AAC features and enables biomarker discovery for LC. The tool is publicly available at https://github.com/Dahrii-Paul/UriPred.

Wnt/β-catenin pathway activation was analyzed by Western blot, and ferroptosis was induced by erastin...KIF23 regulates ATC cell viability, migration, and invasion via the Wnt/β-catenin signaling pathway and ferroptosis. These findings suggest that KIF23 may be a potential therapeutic target for ATC treatment.

An eight-gene CSC signature captures a stemness-linked G2/M program that generalizes across cohorts, relates to the microenvironment, and is therapeutically tractable via kinase targeting, providing a compact readout for risk stratification and preclinical screening.

The model showed robust accuracy (3-year AUC = 0.764) and validation (P = 0.0018). Low-risk patients exhibited enhanced anti-tumor immunity (activated dendritic cells↑, CD8⁺ T cells↑) and heightened sensitivity to bortezomi/venetoclax, etc. We established the lactylation-derived gene signature for MM, providing a clinical tool for risk stratification, immune profiling, and personalized therapy.

This study offers comprehensive insights into ECT2's role in cancer biology through integrative bioinformatics analyses. The results advocate for ECT2 as a potential biomarker and therapeutic target in diverse malignancies, suggesting avenues for personalized oncology strategies.

Overexpression of BUB1 and CCNB2 may enhance cell cycle activity and inflammatory responses, thereby promoting OSCC cell proliferation.

Wnt agonist treatment reversed these effects, and both the Wnt agonist and the mitophagy inhibitor Mdivi-1 were able to rescue the migratory inhibition caused by KIF23 knockdown. KIF23 regulates mitophagy via the Wnt/β-catenin pathway, influencing PTC cell proliferation and migration, suggesting its potential as a therapeutic target for PTC.

We identify several mesenchymal-enriched networks in MBRs associated with focal adhesion, cell matrix, kinase activity, and cell shape/organization, while epithelial-derived MBRs show enriched networks predominantly associated with mitochondrial (processing/transport), midbody, and plasma membrane annotation. Our study sheds light on the proteome architecture of MBRs following oncogenic H-Ras-induced EMT in cell transformation: collectively, our data informs ongoing efforts to delineate oncogenic drivers of cancer initiation, progression, and metastasis.

Extending the analysis to other TCGA cancer types revealed a trend of increased predictive performance on validation data when clinical features were complemented with molecular features, with notable variation between cancer types and clinical endpoints. Our findings suggest that TGFβ signaling genes, prostate cancer related genes and Aurora kinases are strong candidates for patient-specific clinical predictions and could help guide personalized therapeutic decisions.