Ask about this productRelated genes to: CDKN3 antibody
- Gene:
- CDKN3 NIH gene
- Name:
- cyclin dependent kinase inhibitor 3
- Previous symbol:
- -
- Synonyms:
- KAP, CDI1
- Chromosome:
- 14q22.2
- Locus Type:
- gene with protein product
- Date approved:
- 1994-07-04
- Date modifiied:
- 2016-10-05
Related products to: CDKN3 antibody
Related articles to: CDKN3 antibody
- - Source: PubMed
Publication date: 2026/04/18
Wu FanQiao Meng - Men have a higher risk of developing cutaneous squamous cell carcinoma (SCC) compared with women, but models and comprehensive analyses of signaling pathways highlighting this sexual dimorphism are missing. Here, we use a UV-induced SCC model in hairless mice recapitulating this sex difference, with enhanced SCC development in males. While UV-induced DNA damage is similar between sexes, we uncover sex-specific responses in epidermal proliferation and differentiation. Global transcriptional profiling identifies E2F transcription factors as key sex-specific markers of the proliferative response to UV. E2F1/2 and their target gene CDKN3 are selectively downregulated in female mouse and human epidermis following UV exposure, and this is mediated by estrogen receptors. CDKN3 depletion impairs SCC cell progression into S-phase and reduces tumor growth in xenograft models. Consistently, low CDKN3 expression in head and neck SCC occurs exclusively in female patients and correlates with better prognosis. We thus reveal a mechanism protecting women from carcinogen-induced cancer formation, which could lead to better sex-targeted preventive and therapeutic strategies in SCC. - Source: PubMed
Publication date: 2026/03/24
Lukowicz CélineWinkler CarineRoger CatherineFowler Joanna CTsai Yi-ChienMeuli JoachimClaudinot StéphanieChang Yun-TsanIselin ChristophJones Philip HGuenova EmmanuellaJafari ParisMichalik Liliane - Lactylation, a novel post-translational modification in tumor cells, is studied here to explore its relevant gene signature in lung adenocarcinoma (LUAD). - Source: PubMed
Publication date: 2026/03/06
Zhao MingLi BenLi HonghaiNan HaoningSun YafeiPei YanbinZhang XuguangGeng Nan - Paraptosis plays a critical role in mediating anti-tumor effects by inducing cell death in cancer cells. However, its specific involvement in lung adenocarcinoma (LUAD) remains inadequately understood. This study aims to systematically investigate the prognostic significance and underlying mechanisms of paraptosis-related genes (PRGs) in LUAD. Differentially expressed genes were identified between LUAD and control samples from the training set and cross-referenced with PRGs to generate candidate genes (CGs). Prognostic genes were selected from CGs using regression analysis, leading to the development of a LUAD risk model, which was validated in an independent validation set. Clinical characteristics were analyzed to identify independent prognostic factors for constructing a nomogram. Functional and immune infiltration analyses were performed on high-/low-risk cohorts from the training set. Drug predictions related to prognostic genes were made and subsequently validated through molecular docking. Polymerase chain reaction was performed to validate the expression of prognostic genes. Four prognostic genes (CDKN3, PEBP1, TNFRSF19, and PHB) were identified from 27 CGs through regression analysis. The prognostic risk model demonstrated robust predictive capacity for LUAD prognosis and exhibited generalizability. Significant associations were observed between risk scores and clinical features, including age, TNM.stage, T-stage, and N-stage (P < .05). These risk scores served as independent prognostic factors for the nomogram model, offering strong predictive power for LUAD. Vorinostat and raloxifene exhibited notable binding affinity for PEBP1. Elevated CDKN3 expression was observed in LUAD, while PEBP1 and TNFRSF19 expressions were reduced. This study highlights the prognostic value of PRGs, specifically CDKN3, PEBP1, TNFRSF19, and PHB. CDKN3 and PHB emerged as risk factors for LUAD prognosis, whereas PEBP1 and TNFRSF19 did not. In-depth analysis of the tumor microenvironment revealed the distribution and correlations of immune cell types influenced by PRGs and risk score. Furthermore, an independent prognostic model for LUAD was developed, enhancing our understanding of high-/low-risk cohorts' functional pathways. Drug prediction results provided valuable insights into potential therapeutic strategies for LUAD, warranting further investigation. - Source: PubMed
Zhang TaoTang ShugengGuo QuanweiKuang JunYan JunMo YijunTan JianfengWu MengxiLi DongfangZhang Jianhua - Endometrial cancer (EC) ranks among the least prevalent gynecological tumors worldwide, with rising incidence due to aging and obesity. Lymph node metastasis remains common in Uterine Corpus Endometrial Carcinoma (UCEC), necessitating new prognostic biomarkers to guide treatment. In this research, UCEC information from the Cancer Genome Atlas (TCGA) was analyzed, and the results were validated using the Gene Expression Omnibus (GEO). Eighteen differentially expressed genetic factors associated with nicotinamide metabolism (NMRDEGs) were identified. Gene Set Enrichment Analysis (GSEA) indicated their role in oxidative stress, hypoxia, glycolysis, and apoptosis processes. Univariate Cox regression identified six key genes (AURKA, CDKN3, FOXM1, CDKN2A, TK1, and CDK1), utilized to progress a hazard prediction framework. Protein-protein interaction (PPI) analysis uncovered additional hub genes such as CDK2, CCNA2, TP53, and FOXM1. The six key genes showed strong prognostic value, and the study's risk model could guide clinical decisions. Nicotinamide metabolism was found to be significantly linked with EC progression. This study offers new perceptions into the role of nicotinamide metabolism in EC and suggests possible avenues for treatment advancements. - Source: PubMed
Publication date: 2026/01/16
Li YangYu GeLiu LiLiu Shumin