KIFC2 antibody - N-terminal region (ARP33951_P050)
- Known as:
- KIFC2 (anti-) - N-terminal region (ARP33951_P050)
- Catalog number:
- arp33951_p050
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- KIFC2 antibody - N-terminal region (ARP33951_P050)
Related genes to: KIFC2 antibody - N-terminal region (ARP33951_P050)
- Gene:
- KIFC2 NIH gene
- Name:
- kinesin family member C2
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 8q24.3
- Locus Type:
- gene with protein product
- Date approved:
- 2004-01-26
- Date modifiied:
- 2015-08-25
Related products to: KIFC2 antibody - N-terminal region (ARP33951_P050)
Related articles to: KIFC2 antibody - N-terminal region (ARP33951_P050)
- Protein palmitoylation, a reversible post-translational lipid modification, has been implicated in regulating cancer cell signaling and progression; however, its role in prostate cancer (PCa) remains unclear. In this study, we comprehensively analyzed palmitoylation-related genes (PRGs) in PCa by integrating bulk transcriptomic, single-cell RNA sequencing, and spatial transcriptomic datasets. Unsupervised consensus clustering based on PRG expression identified two molecular subtypes with distinct prognoses, immune infiltration profiles, and pathway activities. Differential expression and weighted gene co-expression network analyses revealed five key feature genes, among which KIFC2 was highly expressed in tumor cells and correlated with poor clinical outcomes. The KIFC2 was predominantly enriched in high-grade adenocarcinoma regions. Functional experiments demonstrated that silencing KIFC2 significantly inhibited proliferation and promoted apoptosis in PC3 and DU145 prostate cancer cell lines. Additionally, high KIFC2 expression was associated with increased cell cycle progression and oncogenic signaling pathways, including KRAS and PI3K-AKT. Collectively, these results suggest that palmitoylation and KIFC2 play critical roles in PCa progression and may serve as promising biomarkers and therapeutic targets. - Source: PubMed
Publication date: 2026/01/10
Huang LiangJiang ShusuanZeng FuhuaZeng GongqianShan Hong - - Source: PubMed
Publication date: 2025/08/02
Liu XinyuLin YuLong WeibingYi RenzhengZhang XiongfengXie ChaoqunJin NaQiu ZiranLiu Xiaobing - Hormone receptor-positive and human epidermal growth factor receptor 2-negative breast cancer (HR+/HER2- BC) is the most common subtype, with a high risk of long-term recurrence and metastasis. Endocrine therapy (ET) combined with cyclin-dependent kinase 4/6 (CDK4/6) inhibitors is a standard treatment for advanced/metastatic HR+/HER2- BC, but resistance remains a major clinical challenge. We report that kinesin family member C2 (KIFC2) was amplified in approximately 50% of patients with HR+/HER2- BC, and its high expression was associated with poor disease outcome, increased tumor protein p53 (TP53) somatic mutation, and active pyrimidine metabolism. Functional assays revealed that depletion of KIFC2 suppressed growth and enhanced sensitivity of HR+/HER2- BC cells to tamoxifen and CDK4/6 inhibitors. Mechanistically, KIFC2 stabilized CDK4 by enhancing its interaction with ubiquitin-specific peptidase 9 X-linked (USP9X). Importantly, reexpression of CDK4 in KIFC2-depleted cells partially rescued the decreased growth and increased sensitivity to tamoxifen and CDK4/6 inhibitors caused by KIFC2 depletion. Clinically, high KIFC2 mRNA expression was negatively associated with the survival rate of patients with HR+/HER2- BC who received adjuvant ET alone or in combination with CDK4/6 inhibitors. Collectively, these findings identify an important role for KIFC2 in HR+/HER2- BC growth and therapeutic resistance, and support its potential as a therapeutic target and predictive biomarker. - Source: PubMed
Publication date: 2025/04/29
Yang Shao-YingJin Ming-LiangAndriani LisaZhao QianLing Yun-XiaoLin Cai-JinHuang Min-YingCai Jia-YangZhang Yin-LingHu XinShao Zhi-MingZhang Fang-LinJin XiCao A YongLi Da-Qiang - Studies suggest that kinesin family (KIF) members can promote the occurrence of colorectal cancer (CRC). However, the mechanism of action has not yet been elucidated. The aim of this study was to identify CRC biomarkers associated with KIF members and to investigate their biological mechanisms in the treatment of colorectal cancer by analyzing multi-omics data. CRC-related datasets and KIF member-related genes (KIFRGs) were used. First, differentially expressed genes (DEGs) and differentially expressed methylation genes (DEMGs) in the TCGA-CRC were identified separately using different expression analyses (CRC vs. control). The intersecting genes were selected by overlapping the DEGs, DEMGs, and KIFRGs. Candidate genes were identified using survival analysis ( < 0.05). Subsequently, based on the candidate genes, biomarkers were selected by gene expression validation and survival analysis. Subsequently, functional enrichment, immune cell infiltration, and drug sensitivity analyses were performed. Single-cell analysis was utilized to perform cell annotation, and then function enrichment and pseudo-temporal analyses were performed. The 12 intersecting genes were identified by overlapping 12,479 DEGs, 11,319 DEMGs, and 43 KIFRGs. The survival analysis showed that Kinesin Family Member C2 (KIFC2) and Kinesin Family Member C3 (KIFC3) had significant differences in survival ( < 0.05). Moreover, KIFC3 passed the gene expression validation and survival analysis validation ( < 0.05); thus, KIFC3 was deemed a biomarker. Subsequently, the pathways involved in KIFC3 were detected, such as the Ecm receptor intersection and chemokine signaling pathway. In addition, we found that KIFC3 was significantly positively correlated with natural killer (NK) cells (r = 0.455, < 0.05) and NK T cells (r = 0.411, < 0.05). Moreover, in the drug sensitivity of the CRC, the potential therapeutic benefits of AZD.2281, nilotinib, PD.173074, and shikonin were detected. Furthermore, using single-cell analysis, 16 cell clusters were annotated, and epithelial cells and M2-like macrophages were enriched in "rheumatoid arthritis". Additionally, we observed that most M1-like macrophages were present in the early stages of differentiation, whereas M2-like macrophages were predominant in the later stages of differentiation. This study identifies KIFC3 as a CRC biomarker through multi-omics analysis, highlighting its unique expression, survival association, immune correlations, and drug sensitivity for potential diagnostic and therapeutic applications. - Source: PubMed
Publication date: 2025/04/02
Wang FenZeng XinxinWen JielunXian KexinJin FengJiang SunfangSun Liyue - KIFC2 plays an important role in prostate cancer progression and chemotherapy resistance, but the mechanism of its involvement in other malignancies remains unclear. Therefore, this study aimed to analyze and validate the mechanism of effect of KIFC2 in multiple tumors. Bioinformatic analysis was performed in conjunction with multiple databases (The Cancer Genome Atlas, Genotype-Tissue Expression Project, Human Protein Atlas, etc.) to fully explore the potential role of KIFC2 within individual tumors and to analyze the correlation with major research components such as prognosis, mutations, and the tumor microenvironment. The expression of KIFC2 demonstrates a significant correlation with the prognosis, clinical phenotype, tumor mutational burden, microsatellite instability, and tumor microenvironment across various malignancies and is associated with the modulation of diverse functional and signaling pathways. The differences in the expression of KIFC2 in the bladder cancer tissues (14 pairs) were statistically significant. The pan-cancer analysis in this study revealed the multifunctionality of KIFC2 in a variety of tumors, indicating a possible prognostic predictor and potential therapeutic target for tumors. - Source: PubMed
Publication date: 2024/04/24
Zhang HelinZhang XingxingZhang YuelinHan DaliHa HualanZhang BiaoShang Panfeng