Ask about this productRelated genes to: KIF15 Blocking Peptide
- Gene:
- KIF15 NIH gene
- Name:
- kinesin family member 15
- Previous symbol:
- KNSL7
- Synonyms:
- HKLP2, NY-BR-62
- Chromosome:
- 3p21.31
- Locus Type:
- gene with protein product
- Date approved:
- 2001-12-11
- Date modifiied:
- 2014-11-19
Related products to: KIF15 Blocking Peptide
Related articles to: KIF15 Blocking Peptide
- KIF15, a kinesin-12 family motor protein, has emerged as a recurrently upregulated factor in multiple human malignancies and has been implicated in diverse oncogenic processes. This review aims to provide a comprehensive synthesis of the molecular biology of KIF15, its oncogenic and non-oncogenic functions, the regulatory mechanisms governing its expression and activity, and its therapeutic potential across human disease contexts. - Source: PubMed
Publication date: 2026/05/10
Xiang SumengLi YuxuanZhuang HaihuiLu Ying - Kinesins, a class of microtubule (MT)-dependent molecular motors, regulate MT dynamics and MT-mediated transport. We previously identified Kif15 (kinesin-12) as a key player in axonal growth by modulating MT remodeling during neuronal development, and more recently, its involvement in protein localization. In this study, we observed that Kif15 knockout (Kif15 KO) mice exhibited accelerated functional recovery after sciatic nerve injury. To investigate the cellular responses underlying this enhanced recovery after axotomy, spinal cord tissues from the injured regions were collected for single-nucleus RNA sequencing (snRNA-seq). The snRNA-seq results revealed differential genes expression in neurons, indicating a neuroprotective shift in Kif15 KO mice, and in microglia, where a repair-promoting and synapse-modulating profile was observed. Notably, the CX3CL1-CX3CR1 signaling pathway, critical for neuronal-microglial communication, was downregulated in Kif15 KO mice compared to wild-type controls. Further molecular analysis indicated that Kif15 facilitated the expression and localization of neuronal CX3CL1, which, in turn, influenced microglial function via the receptor CX3CR1. Our findings highlight a novel role for Kif15 in regulating neuronal-microglial communication through modulation of CX3CL1 signaling. - Source: PubMed
Publication date: 2026/04/28
Wu RonghuaZhang WeiQian XiaoweiDong ZhangjiHe XiaomeiZhang SimingChen TaoranYang LiuLiu YanLiu Mei - Kinesin family member 15 (KIF15) is a molecular motor protein that participates in bipolar spindle assembly and centrosome separation during metaphase in normal cells. However, accumulating evidence has shown that KIF15 is aberrantly regulated in the state of malignancy and is associated with the progression of cancers. - Source: PubMed
Publication date: 2026/04/03
Xiang MengqinHu QingLi YanchunWu Hao - Gastric cancer (GC) remains a leading cause of global cancer mortality, necessitating deeper molecular insights. This study identifies KIF15 as a key driver of GC progression through integrated analysis of TCGA data and experimental validation. KIF15 is significantly overexpressed in GC tissues and correlates with advanced tumor stage, metastasis, and poor prognosis. Functional assays demonstrate that KIF15 enhances cancer stem cell (CSC) properties, proliferation, migration, invasion, and cisplatin resistance in GC cells. Mechanistically, KIF15 interacts with peroxiredoxin 1 (PRDX1), stabilizing this antioxidant protein to reduce intracellular hydroperoxides and maintain mitochondrial function. Depletion of PRDX1 reverses KIF15-mediated oncogenic effects. Further investigation reveals Yin Yang 1 (YY1) as the upstream transcriptional activator of KIF15. YY1 directly binds the KIF15 promoter, and its overexpression elevates KIF15 expression. Rescue experiments confirm that YY1 promotes GC malignancy via the KIF15-PRDX1 axis. Crucially, YY1 also transcriptionally regulates PRDX1, forming a coordinated regulatory circuit. In vivo models corroborate that the YY1/KIF15/PRDX1 axis drives tumor growth, metastasis, and chemoresistance. Collectively, these findings establish a novel YY1-KIF15-PRDX1 signaling axis that induces mitochondrial ROS imbalance to facilitate GC progression, offering potential prognostic markers and therapeutic targets. - Source: PubMed
Publication date: 2026/03/30
Li WenjieWu BozhiQian HaishengZhang GuoxinWang XiaoyongLi Xuan - OBJECTIVE: This study aimed to systematically identify and validate KIF15 as a potential diagnostic and prognostic biomarker in colon cancer (CC) using integrated bioinformatics analyses. We further explored its role in the tumor immune microenvironment and its potential value in immunotherapy, and validated its expression and clinical significance through immunohistochemical analysis. METHODS: Gene expression profiles of CC were obtained from the Gene Expression Omnibus (GEO) database to identify differentially expressed genes (DEGs). A protein–protein interaction (PPI) network was constructed, and key genes were identified using the MCODE plugin in Cytoscape. External validation of candidate gene expression was performed using The Cancer Genome Atlas (TCGA) cohort. Kaplan–Meier survival analysis was conducted to evaluate prognostic significance. Receiver operating characteristic (ROC) and time-dependent ROC analyses were applied to assess diagnostic and prognostic performance. A nomogram model was established based on multivariate Cox regression, and its predictive accuracy and stability were evaluated using calibration curves and decision curve analysis (DCA). To investigate the role of KIF15 in the tumor microenvironment, single-cell RNA sequencing data from the TISCH database were analyzed to determine its expression distribution across immune cell subsets. Functional enrichment and immune correlation analyses were performed to elucidate the potential molecular mechanisms of KIF15 in CC progression and to identify downstream hub genes. Finally, immunohistochemistry (IHC) was conducted to validate the tissue expression pattern and clinical relevance of KIF15. RESULTS: A total of 611 DEGs were identified by integrating three GEO datasets (GSE24550, GSE21815, and GSE44076). Based on PPI network construction and MCODE analysis, 13 key genes, including KIF15, were identified. Combined univariate Cox regression and pan-cancer analysis ultimately determined KIF15 as the core gene of interest. TCGA analysis demonstrated that KIF15 was significantly upregulated in CC tissues (P < 0.0001), with a diagnostic ROC AUC of 0.874. Kaplan–Meier analysis showed that high KIF15 expression was significantly associated with poor prognosis (P = 0.004). Multivariate Cox regression confirmed that KIF15 was an independent prognostic factor. The nomogram model constructed based on KIF15 yielded a C-index of 0.783. Time-dependent ROCanalysis showed AUC values of 0.788, 0.777, and 0.712 for 1-, 3-, and 5-year survival, respectively. Calibrationcurves and DCA indicated good predictive consistency and clinical net benefit. Single-cell analysis revealedthat KIF15 was highly expressed in proliferating T cells (Tprolif). Functional enrichment analysis indicatedthat KIF15 was primarily involved in the cell cycle, DNA replication, mitosis, and the p53 signaling pathway.Immune correlation analysis showed significant associations between KIF15 expression and multipleimmune-infiltrating cells as well as immune checkpoint genes. Four downstream hub genes (TTK, CDK1,CHEK1, and KIF2C) were further identified and were all significantly upregulated in CC. IHC results confirmedthat KIF15 was highly expressed in CC tissues (P < 0.001) and was significantly associated with poorprognosis. Pearson correlation analysis demonstrated that KIF15 expression was positively correlated withimmune markers, including PD-1 and PD-L1. CONCLUSION: KIF15 is significantly overexpressed in CC tissues and is strongly associated with unfavorable prognosis, suggesting its potential clinical value in the diagnosis and prognostic assessment of CC. Notably, KIF15 expression is closely correlated with immune cell infiltration and multiple immune checkpoint molecules, indicating a potential role in regulating the tumor immune microenvironment. Therefore, KIF15 may serve as a promising biomarker and potential therapeutic target for immunotherapy, as well as a candidate marker for diagnosis, prognosis evaluation, and individualized treatment in CC. - Source: PubMed
Publication date: 2026/03/23
Wu HuimingXue DingwenLi XiaoyuDeng MinGuo RenkaiJin ChenfeiCui YipengLuo FeiXue LiangLi Huiyu