No abstract available.
Carcinoma, Renal Cell* ; Caveolin 1*

For lack of the biomarker, early diagnosis of prostate cancer is often difficult. Caveolin-1 (Cav-1) is an important oncogene and a major structural coat protein of caveolae, which is involved in multiple cellular functions including molecular transport, cell adhesion, and signal transduction, as well as in the development and progression of prostate cancer. Cav-1 is secreted as a biologically active molecule that promotes cell survival and angiogenesis within the tumor microenvironment, and is overexpressed in the metastatic and primary sites of human prostate cancer. Secreted Cav-1 can be detected in the peripheral blood, and its expression level has an indicative value in the diagnosis and prognosis of prostate cancer. This review focuses on the structure and biological characteristics of Cav-1 and its correlation with prostate cancer.
Biomarkers, Tumor ; Caveolin 1 ; Humans ; Male ; Prostatic Neoplasms ; diagnosis

Autophagy, is an essential cellular process involving self-degradation of intracellular components via the lysosome, which plays the Janus role in cancer initiation and progression. Caveolin-1, a marker protein of caveolae, functions as scaffolding protein mediating many physiological and pathological processes including caveolae biogenensis, vesicular transport, cholesterol homeostasis, signal transduction and tumorigenesis. Recently, many reports showed that autophagy of tumor cells associated with stromal Cav-1. We reviewed that the relationship between autophagy and Cav-1 involved in tumorigenesis and development.
Animals ; Autophagy ; physiology ; Caveolin 1 ; physiology ; Humans ; Neoplasms ; pathology ; physiopathology

OBJECTIVETo investigate the protein expression of caveolin-1 in type II alveolar epithelial cells (A549) exposed to carbon black nanoparticles (CB NPs) and the role of caveolin in the endocytosis of CB NPs.

METHODSA549 cells were exposed to 0, 25, 50, 100, 200, and 400 µg/ml CB NPs for 24 h; then, trypan blue assay was applied to determine the cell viability. A549 cells were also exposed to 0, 25, 50, and 100 µg/ml CB NPs for 24 h, then, transmission electron microscopy (TEM) and flow cytometry were applied to observe the morphological change of cells and cellular side scatter (SSC), and Western blot was used to analyze the effect of CB NPs on the protein expression of caveolin-1. A549 cells were co-exposed to1 µg/ml filipin and 100 µg/ml CB NPs for 24 h, then, the cellular SSC was observed.

RESULTSCompared with controls, the A549 cells exposed to 200 and 400 µg/ml CB NPs had the cell viability decreased by 38.2% and 46.6%, respectively (P < 0.05), while those exposed to 25, 50, and 100 µg/ml CB NPs showed no significant decrease in cell vitality (P > 0.05). The protein expression of caveolin-1 was significantly higher in the cells exposed to 50 and 100 µg/ml CB NPs than in controls (P < 0.05). The TEM showed that plasmalemmal vesicles containing black particles were found in the cytoplasm of the cells exposed to 50 and 100 µg/ml CB NPs. The flow cytometry showed that the cellular SSC ratio increased from 1.007 to 1.331 as the dose of CB NPs rose within 0 ∼ 100 µg/ml and fell to 1.25 after the cells were co-exposed to1 µg/ml filipin and 100 µg/ml CB NPs.

CONCLUSIONCarbon black nanoparticles can be transferred into A549 cells by endocytosis, but caveolin-mediated endocytic pathway plays a minor role in this process.

Caveolin-1 (Cav-1) is a trans-membrane protein that is a major component of the caveolae structure on the plasma membrane. Cav-1 is involved in the regulation of various cellular processes, including cell growth, differentiation, endocytosis, and in particular it has been implied in cellular senescence. Here we review current knowledge about Cav-1 in cellular signaling and discuss the role of Cav-1 in aging-related diseases.
Caveolae ; Caveolin 1 ; Cell Aging ; Cell Membrane ; Endocytosis

The expression of caveolin-1 and -2 in the retina was examined; Western blot analysis showed that both were present. Immunohistochemistry indicated that caveolin-1 was expressed in the majority of retinal layers, including the ganglion cell layer, inner plexiform layer, outer plexiform layer, and in the vascular endothelial cells of the retina. Caveolin-2 was primarily immunostained in the vessels, but in a few other elements as well. This is the first demonstration of caveolin differential expression in the retina of rats, and suggests that caveolin plays an important role in signal transduction in glial cells and neuronal cells.
Animals ; Caveolin 1/*analysis/immunology ; Caveolin 2/*analysis/immunology ; Gene Expression Regulation ; Immunohistochemistry ; Male ; Rats ; Rats, Sprague-Dawley ; Retina/*chemistry

PURPOSE: Renal tumors consist of heterogeneous groups that frequently show complex and overlapping morphology, thus making it difficult to make a correct diagnosis. One of the most problematic differential diagnoses is to distinguish chromophobe renal cell carcinoma (RCC) from oncocytoma. These should be distinguished by differences in their behavior and clinical outcome. Our study was performed to identify whether caveolin-1 and MOC-31 are useful immunohistochemical markers for differentiating chromophobe RCC from oncocytoma. MATERIALS AND METHODS: We selected 23 chromophobe RCCs, 8 oncocytomas, and 25 clear cell RCCs and performed immunohistochemical staining for caveolin-1 and MOC-31. RESULTS: Caveolin-1 was positive in 20 (87%) of 23 chromophobe RCCs, 0 of 8 oncocytomas, and 21 (84%) of 25 clear cell RCCs. MOC-31 was positive in 22 (96%) of 23 chromophobe RCCs, 2 (25%) of 8 oncocytomas, and 14 (56%) of 25 clear cell RCCs. There was a statistically significant difference in the expression of caveolin-1 and MOC-31 between chromophobe RCC and oncocytoma (p<0.001). In addition, clear cell RCC was also significantly different from oncocytoma in the expression of caveolin-1 (p<0.001) and was significantly different from chromophobe RCC in the expression of MOC-31 (p<0.001). CONCLUSIONS: Caveolin-1 and MOC-31 can be useful markers in the differential diagnosis of chromophobe RCC, oncocytoma, and clear cell RCC.
Adenoma, Oxyphilic ; Antibodies, Monoclonal ; Carcinoma, Renal Cell ; Caveolin 1 ; Diagnosis, Differential ; Kidney Neoplasms

BACKGROUND: Nitric oxide (NO) in articular chondrocytes regulates dedifferentiation and inflammatory responses by modulating MAP kinases. In this study, we investigated whether the Src kinase in chondrocytes regulates NO-induced dedifferentiation and cyclooxygenase-2 (COX-2) expression. METHODS: Primary chondrocytes were treated with various concentrations of SNP for 24 h. The COX-2 and type II collagen expression levels were determined by immunoblot analysis, and prostaglandin E(2) (PGE(2)) was determined by using a PGE(2) assay kit. Expression and distribution of p-Caveolin and COX-2 in rabbit articular chondrocytes and cartilage explants were determined by immunohistochemical staining and immunocytochemical staining, respectively. RESULTS: SNP treatment stimulated Src kinase activation in a dose-dependent manner in articular chondrocytes. The Src kinase inhibitors PP2 [4-amino-5-(4-chlorophenyl)-7-(t-butyl)pyrazolo(3,4-d)pyrimidine], a significantly blocked SNP-induced p38 kinase and caveolin-1 activation in a dose-dependent manner. Therefore, to determine whether Src kinase activation is associated with dedifferentiation and/or COX-2 expression and PGE(2) production. As expected, PP2 potentiated SNP-stimulated dedifferentiation, but completely blocked both COX-2 expression and PGE2 production. And also, levels of p-Caveolin and COX-2 protein expression were increased in SNP-treated primary chondrocytes and osteoarthritic and rheumatoid arthritic cartilage, suggesting that p-Caveolin may play a role in the inflammatory responses of arthritic cartilage. CONCLUSION: Our previously studies indicated that NO caused dedifferentiation and COX-2 expression is regulated by p38 kinase through caveolin-1 (1). Therefore, our results collectively suggest that Src kinase regulates NO-induced dedifferentiation and COX-2 expression in chondrocytes via p38 kinase in association with caveolin-1.
Cartilage ; Caveolin 1 ; Chondrocytes* ; Collagen Type II ; Cyclooxygenase 2* ; Dinoprostone ; Nitric Oxide ; Phosphotransferases*

PURPOSE: We investigated the relationship between the expression of caveolin-1, using a tissue microarray (TMA), and the prognosis of patients with renal cell carcinoma (RCC). MATERIALS AND METHODS: TMA sections of formalin-fixed, paraffin-embedded tissues of RCC from 82 patients, who had undergone radical nephrectomy, were stained immunohistochemically with specific antibodies against caveolin-1. The caveolin-1 immunostaining was semi-quantitatively estimated based on intensity. The expression pattern of caveolin-1 was compared with the clinicopathological variables. RESULTS: The expression of caveolin-1 was significantly correlated with tumor size (p=0.002), TNM stage (p<0.001), T stage (p=0.001), M stage (p=0.004), grade (p=0.028) and metastasis (p<0.001), and was also significantly higher in clear cell than non-clear cell RCC (p<0.001). The survival of patients with higher caveolin-1 expression was significantly worse than that of patients with lower caveolin-1 expression (p=0.001). Univariate analyses were able to identify all variables, including caveolin-1 expression as significant prognostic factors for cancer-specific survival; multivariate analyses indicated that TNM stage, M stage and grade were independent prognostic factors. Caveolin-1 expression was not an independent factor. CONCLUSIONS: The increased expression of caveolin-1 is associated with tumor size, stage, grade, metastasis and a worse prognosis in RCC, which suggests that caveolin-1 may be important in the progression of RCC.
Antibodies ; Carcinoma, Renal Cell* ; Caveolin 1* ; Humans ; Multivariate Analysis ; Neoplasm Metastasis ; Nephrectomy ; Prognosis*

BACKGROUND/AIMS:: We demonstrated the role of caveolin-1 involved in high glucose (HG)-induced glomerular mesangial cells (GMCs) senescence. METHODS:: HG was used to stimulate GMCs. The telomere lengths were analyzed by Southern blot. β-Galactosidase staining was determined. The expressions of caveolin-1 and P53 proteins were determined by Western blot. RESULTS:: Treatment with high concentrations of glucose induced GMC senescence accompanied by shortened telomere length and increase of β-galactosidase staining as well as P53 protein, which was abrogated after application of caveolin-1-siRNA. CONCLUSIONS:: This study proved that HG induced cell senescence in GMCs. The caveolin-1 is involved in HG-induced mesangial cell senescence, and blocking caveolin-1 significantly reduced cell senescence. The effect of caveolin-1 is mediated by P53 pathway.
Aging* ; Blotting, Southern ; Blotting, Western ; Caveolin 1* ; Cell Aging ; Glucose* ; Humans* ; Mesangial Cells* ; Telomere