KPNA2 (Karyopherin Subunit Alpha 2)

Single-cell analysis further localized this axis to a proliferative mitotic subpopulation, promoting melanoma progression. These findings uncover a previously unrecognized mechanism by which KA inhibits melanoma growth and suggest that targeting the MYC-CCNA2/KPNA2 pathway may provide a therapeutic strategy for melanoma.

Furthermore, the identified biomarker CDCA8 represents a promising therapeutic target warranting further investigation. These discoveries provide novel evidence on senescence in HCC, which may tailor the pharmacological interventions to improve the clinical management.

High-risk patients exhibited enriched HIF-1/VEGF signaling, elevated TMB, immunosuppressive microenvironments, and increased TIDE scores. ISG15 knockdown suppressed proliferation, migration, and invasion in ccRCC cells by promoting KPNA2 ubiquitination and degradation, which was rescued by KPNA2 overexpression.

A CRC risk model based on 6 AS-related genes was developed, identifying 3 novel AS genes. It highlights shared genetic factors, offering prognostic biomarkers for both diseases and insights into their interconnected mechanisms.

Our study reveals HDAC5/H3K27ac/KPNA2 axis as the anti-metastatic mechanism of TBMS1 in cervical cancer, suggesting TBMS1 serves as a promising drug for cervical cancer treatment.

Furthermore, we observed a reduction in FOXM1 expression following the suppression of KPNA2. These findings indicate the presence of a positive feedback loop between the expression of KPNA2 and FOXM1, which contributes to an enhanced proliferation of lung adenocarcinoma cells.

The characteristics of circCOL5A1 were verified by RNase R and actinomycin D experiments, and its subcellular localization was analyzed by PARIS kit...CircCOL5A1 promoted cell proliferation, migration, invasion, EMT and glycolysis by cytoplasmic adsorption of miR-3940-3p and up-regulation of KPNA2 in RCC. CircCOL5A1 is anticipated to be a promising molecular target for diagnosing and treating RCC.

The findings of this study have significant clinical implications, suggesting that our nine-gene prognostic model could be integrated into routine clinical practice to enhance patient stratification and inform treatment decisions for COAD. Future research should focus on prospective validation and exploration of therapeutic targets within the identified genes.

This effect was attributed to the regulation of c-MYC nuclear translocation through KPNA2 deubiquitination. The findings underscore the imperative for further evaluation of the potential therapeutic significance of USP14 in gastric cancer.

Thus, this study revealed potential diagnostic and prognostic signatures based on comprehensive analyses of BC patient data sourced from The Cancer Genome Atlas database. Consequently, four gene signatures were constructed: two differentiate ER+ from ER-BC: TTC8, SLC5A7, and PLCH1 for overall survival (OS); ZNF695, SLC7A5, and PLCH1 for disease free survival (DFS), while the other two effectively distinguish tumor from normal samples: SPC25, ANLN, KPNA2, SLC7A5 for OS; SPC25, KIF20A, SKA3, DTL, CDCA3, ANLN, TTK, RAD54L, MYBL2, ZNF695, and SLC7A5 for DFS.

The model also demonstrated associations with immune cell infiltration and drug sensitivity, highlighting its potential utility in optimizing immunotherapy and chemotherapy strategies. This study developed a novel ARG-based prognostic model that aids in survival prediction and therapeutic decision-making for metastatic melanoma patients. DOCK10 was identified as a potential therapeutic target in melanoma metastasis.

Specifically, O-GlcNAcylation enhances UGDH interaction with KPNA2 to compete with STAT1, and suppresses translocation of STAT1 into the nucleus, thereby transcriptionally downregulating CXCL10 expression. Thus, our study identifies UGDH O-GlcNAcylation as a key regulator of tumor immunity and further suggests a potential strategy for enhancing immunotherapy.