Ask about this productRelated genes to: CAV1 antibody
- Gene:
- CAV1 NIH gene
- Name:
- caveolin 1
- Previous symbol:
- CAV
- Synonyms:
- -
- Chromosome:
- 7q31.2
- Locus Type:
- gene with protein product
- Date approved:
- 1993-11-02
- Date modifiied:
- 2016-10-05
Related products to: CAV1 antibody
Related articles to: CAV1 antibody
- Tumor immunity is a crucial defense mechanism that suppresses tumor initiation and delays tumor progression. The interplay between tumor metabolic reprogramming and immune evasion is a putative determinant in the tumor progression. Caveolin-1 (Cav-1) is a major biomarker of caveolae and is involved in cell signaling, lipid metabolic reprogramming, and antitumor immune responses. Cav-1 is widely expressed in immune cells and tumor cells, with frequent upregulation in breast cancer, liver cancer, lung cancer, pancreatic cancer, glioma, and melanoma. However, Cav-1 expression is context-dependent and varies across cancer subtypes, including gastric cancer. This review discusses the structure and functions of Cav-1, emphasizing its role in tumor-associated immune cells. We summarized Cav-1-mediated lipid metabolic reprogramming regulates antitumor immunity and highlighted challenges in developing Cav-1-targeting drugs. Notably, tumor cell metabolic reprogramming not only supports cancer cell progression but also drives immunosuppression via inhibitory cytokines like transforming growth factor-β (TGF-β) and interleukin-4 (IL-4), fostering immune evasion and therapy resistance. While Cav-1 represents a potential biomarker and therapeutic target, its heterogeneous expression and context-specific functions necessitate further research to develop precise therapies. Future investigations into the mechanisms of Cav-1 in tumor immunity may pave the way for more effective cancer treatments. - Source: PubMed
Publication date: 2026/05/04
Ge XiyueSong TianyiGuo XiangyanLi JiajieWang ZenghuaShi YaningQin LiZhang Chanjuan - High-Grade Serous Ovarian Cancer (HGSOC) is the most lethal gynecological malignancy due to aggressive growth, widespread metastases, and high intra-tumoral heterogeneity. Poor prognosis is largely due to late diagnosis, hence there is an urgent need to identify novel biomarkers for screening, diagnosis, and monitoring. Here, we propose the voltage-dependent calcium channel hCaV1.2 encoded by CACNA1C as a potential biomarker and therapeutic target in HGSOC. Using IHC analysis for ten ovarian cancer patients, cytotoxicity assay, TCGA gene expression and survival analyses, homology modeling, molecular docking, Calcium channel membrane assembly and molecular dynamics simulations, we tested CACNA1C's role in HGSOC progression and the effect of blocking on cancer cell survival. We show that nifedipine (NIFE), a calcium channel blocker (CCB), had a tumor suppressive effect based on binding models predicted by three-dimensional computer assisted molecular modeling and in vitro validation using human HGSOC cell line. Using The Cancer Genome Atlas ovarian public cohort, we found CACNA1C mRNA expression strongly correlated with poor patient survival for late-stage and metastasis than primary. We also show strong correlation of CACNA1C protein expression using immunohistochemistry correlating with COH ovarian carcinomas patients' disease progression. This research demonstrates that targeting HGSOC via CCBs may be therapeutically beneficial. By establishing further in vitro, in vivo, and clinical trials using FDA approved NIFE may be repurposed to target CACNA1C for HGSOC. - Source: PubMed
Publication date: 2026/04/22
Hammad Mohamed AWu Kingsley YAbd El-Fattah Eslam EAboody Karen SChang Chia-En A - Glutaminase 1 (GLS1) drives glutaminolysis to support tumor growth and survival, yet its role in the tumor microenvironment remains poorly understood. Here, we demonstrate that GLS1 promotes angiogenesis in head and neck squamous cell carcinoma (HNSCC) via an exosome-dependent mechanism. In HNSCC xenograft models, genetic silencing of GLS1 or treatment with CB-839 markedly reduces intratumoral angiogenesis. Exosomes from GLS1-deficient cells impair endothelial cell migration and tube formation compared with control exosomes. Proteomic analysis reveals a loss of the pro-angiogenic protein Tenascin C (TNC) in GLS1-deficient exosomes. Mechanistically, loss of GLS1 interferes with USP1-mediated deubiquitination of Caveolin-1 (CAV1), resulting in CAV1 degradation and impaired recruitment of TNC into exosomes. Exosomes deficient in CAV1-TNC complexes subsequently disrupt integrin-dependent FAK-SRC signaling in endothelial cells, inhibiting their angiogenic activity. Collectively, these findings uncover a non-metabolic role of GLS1 in promoting tumor angiogenesis through exosome-mediated CAV1-TNC signaling, suggesting that targeting GLS1 may simultaneously inhibit tumor metabolism and angiogenesis in HNSCC. - Source: PubMed
Publication date: 2026/05/03
Yang JianqiangFu ZhenzhenChen FanghuiVijaya Kumar SoumyaYang FanZheng YaochaoLi YunqiYao YaoSaba Nabil FTeng Yong - Bladder outlet obstruction (BOO) leads to detrusor overactivity (DO) and structural remodeling of the bladder. However, the molecular mechanisms underlying this process remain incompletely understood. - Source: PubMed
Yu Seong HyeonChung Ho SeokLim Do GyeongKim Sun-Ouck - Currently, there are few studies exploring the expression of Caveolin-1 (CAV-1) in breast cancer tissues and its clinicopathological significance using immunohistochemistry (IHC) technology. This study detected the expression of CAV-1 in 300 cases of invasive breast cancer paraffin tissues through IHC, and analyzed the relationship between CAV-1 expression and the clinicopathological characteristics and prognosis of breast cancer patients. Our results showed that the positivity rate of CAV-1 in breast cancer tissues was 10.0% (30/300), significantly higher than that in normal breast tissues (0.0%, 0/58) ( = 0.024). CAV-1 expression was higher in breast cancer with larger tumors, higher tumor grade, ER negative, PR negative, HER2 negative, higher Ki-67 index, and triple-negative breast cancer (TNBC) molecular subtype (all < 0.05); however, the positivity rate of CAV-1 in breast cancer without axillary lymph node metastasis (13.6%, 21/154) was significantly higher than that in patients with axillary lymph node metastasis (4.9%, 7/143) ( = 0.010). In multiple logistic regression analysis, the independent predictor of CAV-1 expression in breast cancer was TNBC status (odds ratio = 32.099; 95% confidence interval: 9.341-110.302; < 0.001). We further analyzed the value of CAV-1 in distinguishing between TNBC and non-TNBC, the results showed that the sensitivity, specificity, positive predictive value (PPV), and negative predictive value (NPV) of CAV-1 positive prediction for TNBC were 32.9%, 98.6%, 90.0%, and 79.5%, respectively. Regardless of all breast cancer or TNBC patients, no clear relationship was observed between patient prognosis and CAV-1 expression. We suggest that CAV-1 expression is significantly upregulated in TNBC, with potential clinical value for distinguishing between TNBC and non-TNBC. - Source: PubMed
Publication date: 2026/04/15
Wang Chao-QunShao Jun-KangWang YanLu Shi-PingXu Zheng-GuoHu Chao-HuiHuang Bi-Fei