Objective To investigate the effect of caveolion-1 on the growth and proliferation in human breastcancer MCF7 cell in vitro and in vivo and approach its mechanisms. Methods The plasmid pCI-neo-cav-1 and its corres-ponding empty vector （pCI-neo） were transfected into MCF7 cell line. The expressions of caveolin-1 and vascular endoth-elial growth factor （VEGF） in transfectants were subsequently confirmed by Western blot analysis. A pair of monoclonal cell lines， MCF7/cav-1 and MCF7/vec， were chose for future studies. The colony formation ability of tumor cells was detected by anchorage-independent growth assay. Xenograft tumor models in nude mice were established. Immunohisto-chemistry was used to characterize Ki-67 and VEGF levels in the tumors tissues. Results Caveolin-1 expression was up-regulated in the MCF7/cav-1 cell as compared with the MCF7/vec cell （P＜0.01） and the MCF7 cell （P＜0.01）. Caveolin-1 overexpression markedly reduced the capacity of the cells to form colonies in soft agar （P＜0.01）. Compared with the MCF7/vec cell， VEGF protein expression reduced in the MCF7/cav-1 cell （P＜0.01）. In vivo experiments in nude mice， the overexpression of caveolin-1 resulted in significant growth inhibition of the xenograft breast tumors. The Ki-67 staining was weak and the VEGF staining was negative by immunohistochemistry that indicated the caveolin-1 inhibited the proliferation in human breast cancer MCF7 cell. Conclusion The caveolin-1 might inhibit the growth and proliferation in human breast cancer MCF7 cell through suppressing activation of VEGF signaling pathway.
ObjectiveTo investigate the effect and mechanism of caveolion-1 on the growth and proliferation of human pancreatic carcinoma cell Panc1, in vitro. MethodsThe plasmid pCI-neo-cav-1 and its corresponding empty vector (pCI-neo) were transfected into Panc1 cell line (study group and control group, respectively). Expressions of caveolin-1, Akt, and Aktphosphate (p-Akt) were determined in transfectants by Western blot analysis. The cell growth curve was drawn and the double time was calculated in each group, and the cell cycle was analyzed by flow cytometry. The colony formation ability of tumor cells was detected by anchorageindependent growth assay. ResultsCaveolin-1 expression was up-regulated (Plt;0.01) and the growth of Panc1 cell was inhibited significantly (Plt;0.01) in the study group comparing with the control group. Caveolin-1 overexpression inhibited proliferation of Panc1 cell by arresting the cell cycle in the G0/G1 phase (Plt;0.05), the rate of S phase in the study group was lower than that of the control group (Plt;0.01). Proliferation index of the study group was also lower than that of the control group (Plt;0.01). Caveolin-1 overexpression reduced the capacity of the cells to form colonies in soft agar (Plt;0.01). p-Akt protein was reduced in the study group as compared with the control group (Plt;0.05). ConclusionCaveolin-1 can function as a cancer suppressor through inhibiting the activation of PI3K/Akt signaling pathway in Panc1 cell.
Caveolin-1 (Cav-1) protein plays a very important role in the central nervous system, and is closely related to Alzheimer’s disease (AD). Through literature review, this article summarizes the present research status of Cav-1 protein in the field of AD from three aspects: the relationship between Cav-1 gene and AD; the relationship of Cav-1 protein with learning and memory; the relationship of Cav-1 protein with amyloid β-protein and Tau protein. And the aim of this paper is to provide a new thought and evidence for exploring the mechanism of AD via Cav-1 protein.
Objective To investigate the effects of caveolin-1 scaffolding domain peptide ( CSD-p)on expressions of extracellular matrix and Smads in human fetal lung fibroblasts. Methods Human fetal lung fibroblasts were cultured in vitro and divided into four groups. A control group: the cells were cultured in DMEMwithout TGF-β1 or CSD-p. A CSD-p treatment group: the cells were cultured in DMEMcontaining 5 μmol /L CSD-p. A TGF-β1 treatment group: the cells were cultured in DMEMcontaining 5 μg/L TGF-β1 .A TGF-β1 + CSD-p treatment group: the cells were cultured in DMEM containing 5 μg/L TGF-β1 and 5 μmol /L CSD-p. Caveolin -1 mRNA was detected by RT-PCR. Caveolin-1, collagen-Ⅰ, α-SMA, p-Smad2,p-Smad3 and Smad7 proteins were measured by Western blot. Results Compared with the control group,the Caveolin -1 mRNA and protein expressions in the cells of TGF-β1 group significantly reduced ( mRNA:0. 404 ±0. 027 vs. 1. 540 ±0. 262; protein: 0. 278 ±0. 054 vs. 1. 279 ±0. 085; P lt; 0. 01) , and the expression levels of collagen-Ⅰ and α-SMA proteins significantly increased ( collagen-Ⅰ: 1. 127 ±0. 078 vs.0. 234 ±0. 048; α-SMA: 1. 028 ±0. 058 vs. 0. 295 ±0. 024) . Meanwhile, the expression levels of p-Smad2 ( 1. 162 ±0. 049 vs. 0. 277 ±0. 014) and p-Smad3 proteins ( 1. 135 ±0. 057 vs. 0. 261 ±0. 046) increased with statistical significance ( P lt; 0. 01) , but the expression level of Smad7 protein significantly reduced( 0. 379 ±0. 004 vs. 1. 249 ±0. 046, P lt;0. 001) . In the CSD-p group, CSD-p had no significant effects on the expressions of above proteins compared with the control group. But in the TGF-β1 +CSD-p group, the overexpressions of collagen-Ⅰ, α-SMA, p-Smad2 and p-Smad3 induced by TGF-β1 were obviously inhibited by CSD-p ( collagen-Ⅰ: 0. 384 ±0. 040 vs. 1. 127 ±0. 078; α-SMA: 0. 471 ±0. 071 vs. 1. 127 ±0. 078;p-Smad2: 0. 618 ±0. 096 vs. 1. 162 ±0. 049; p-Smad3: 0. 461 ±0. 057 vs. 1. 135 ±0. 057; P lt; 0. 01) .Otherwise, the up-regulation of Smad7 ( 0.924 ±0. 065 vs. 0.379 ±0. 004) was found. Conclusions CSD-p can reduce fibroblast collagen-I and α-SMA protein expressions stimulated by TGF-β1 , possibly through regulation of TGF-β1 /Smads signaling pathway. It is suggested that an increase in caveolin -1 function through the use of CSD-p may be an intervention role in pulmonary fibrosis.
Objective To systematically evaluate the association between Caveolin-1 and gastric cancer, as well as its clinical pathologic features. Methods Databases including Wanfang, VIP, CNKI and PubMed were searched to identify case-control studies involving the association between Caveolin-1 and gastric cancer as well as its clinical pathologic features from January 2000 to May 2017. The literatures were screened and the methodological quality was assessed, then RevMan 5.3 software was used to conduct Meta-analysis. Results A total of 12 case-control studies were collected after screening, including 1 380 cases of gastric cancer, with Caveolin-1 expressed positive in 286 cases; 295 cases of non-carcinoma control, with Caveolin-1 expressed positive in 264 cases; 238 cases of precancerous lesions of gastric cancer, with Caveolin-1 expressed positive in 180 cases. Results of Meta-analysis indicated that: as for Caveolin-1 expression, significant differences were found in non-carcinoma vs. gastric cancer [odds ratio (OR)=23.74, 95% confidence interval (CI) (15.19, 37.11), P<0.000 01], precancerous lesions of gastric cancer vs. gastric cancer [OR=6.58, 95%CI (4.52, 9.58), P<0.000 01], and non-carcinoma control vs. precancerous lesions of gastric cancer [OR=2.88, 95%CI (1.58, 5.25), P=0.000 6]. Significant differences were also found between Caveolin-1 expression and gastric cancer clinical pathologic features in undifferentiated vs. differentiated tissue [OR=0.48, 95%CI (0.33, 0.70), P=0.000 1], and without vs. with lymph node metastasis [OR=3.19, 95%CI (1.77, 5.74), P=0.000 1]. Conclusions Caveolin-1 expression is lesser in most gastric cancer patients than in the controls, and is closely associated with its clinical pathologic features. Due to limited quantity and quality of included studies, more high quality studies are needed to verify the conclusion of Caveolin-1 as a tumor marker in gastric cancer.