Prognostic Value of Caveolin-1 Expression in Gastric Cancer: a Meta-analysis

Yang, Yue; Miao, Shuhan; Lu, Rongzhu; Zhou, Jianwei

doi:10.7314/apjcp.2014.15.19.8367

Cited by 12 publications

(7 citation statements)

References 16 publications

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“…In addition, Yang et al reported that increased Cav-1 expression was associated with prolonged overall survival rate in hepatocellular carcinoma ( P = 0.021) [113]. Similar findings were also confirmed on breast cancer [99] and gastric cancer patients [114]. In particular, our analysis also revealed a close link between Cav-1 and lung cancer.…”

Section: Emerging Role Of Cav-1 In Cancer Preventionsupporting

confidence: 87%

Caveolin‐1: An Oxidative Stress‐Related Target for Cancer Prevention

Wang

Zheng

et al. 2017

Oxidative Medicine and Cellular Longevity

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Aberrant oxidative metabolism is one of the hallmarks of cancer. Reactive species overproduction could promote carcinogenesis via inducing genetic mutations and activating oncogenic pathways, and thus, antioxidant therapy was considered as an important strategy for cancer prevention and treatment. Caveolin-1 (Cav-1), a constituent protein of caveolae, has been shown to mediate tumorigenesis and progression through oxidative stress modulation recently. Reactive species could modulate the expression, degradation, posttranslational modifications, and membrane trafficking of Cav-1, while Cav-1-targeted treatments could scavenge the reactive species. More importantly, emerging evidences have indicated that multiple antioxidants could exert antitumor activities in cancer cells and protective activities in normal cells by modulating the Cav-1 pathway. Altogether, these findings indicate that Cav-1 may be a promising oxidative stress-related target for cancer antioxidant prevention. Elucidating the underlying interaction mechanisms between oxidative stress and Cav-1 is helpful for enhancing the preventive effects of antioxidants on cancer, for improving clinical outcomes of antioxidant-related therapeutics in cancer patients, and for developing Cav-1 targeted drugs. Herein, we summarize the available evidence of the roles of Cav-1 and oxidative stress in tumorigenesis and development and shed novel light on designing strategies for cancer prevention or treatment by utilizing the interaction mode between Cav-1 and oxidative stress.

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Section: Emerging Role Of Cav-1 In Cancer Preventionsupporting

confidence: 87%

Caveolin‐1: An Oxidative Stress‐Related Target for Cancer Prevention

Wang

Zheng

et al. 2017

Oxidative Medicine and Cellular Longevity

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“…It has also been directly linked to the metastatic potential of pancreatic cancer cells through the regulation of epithelial to mesenchymal transition (EMT), a phenomenon closely related to the metastatic potential and chemoresistance of cancer cells (15,16). Nevertheless, conflicting results have been presented (17), with the loss of Cav-1 in the tumor stroma being associated with an adverse clinical outcome in a variety of cancer types (18-23).…”

Section: Introductionmentioning

confidence: 99%

Silencing of caveolin-1 in fibroblasts as opposed to epithelial tumor cells results in increased tumor growth rate and chemoresistance in a human pancreatic cancer model

et al. 2018

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Caveolin-1 (Cav-1) expression has been shown to be associated with tumor growth and resistance to chemotherapy in pancreatic cancer. The primary aim of this study was to explore the significance of Cav-1 expression in pancreatic cancer cells as compared to fibroblasts in relation to cancer cell proliferation and chemoresistance, both in vitro and in vivo, in an immunodeficient mouse model. We also aimed to evaluate the immunohistochemical expression of Cav-1 in the epithelial and stromal component of pancreatic cancer tissue specimens. The immunohistochemical staining of poorly differentiated tissue sections revealed a strong and weak Cav-1 expression in the epithelial tumor cells and stromal fibroblasts, respectively. Conversely, the well-differentiated areas were characterized by a weak epithelial Cav-1 expression. Cav-1 downregulation in cancer cells resulted in an increased proliferation in vitro; however, it had no effect on chemoresistance and growth gain in vivo. By contrast, the decreased expression of Cav-1 in fibroblasts resulted in a growth advantage and the chemo-resistance of cancer cells when they were co-injected into immunodeficient mice to develop mixed fibroblast/cancer cell xenografts. On the whole, the findings of this study suggest that the downregulation of Cav-1 in fibroblasts is associated with an increased tumor proliferation rate in vivo and chemoresistance. Further studies are warranted to explore whether the targeting of Cav-1 in the stroma may represent a novel therapeutic approach in pancreatic cancer.

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“…Recent studies reported that the loss of CAV1 in the tumor stroma results in an activated tumor microenvironment and was significantly related to metastasis, early tumor recurrence, and poor clinical outcome in breast cancer, prostate cancer, and other solid tumors 32 , 38 – 41 . Simultaneously, high CAV1 expression could predict a better overall survival in gastric cancer in a meta-analysis 42 .…”

Section: Resultsmentioning

confidence: 97%

Quantitative proteomic Analysis Reveals up-regulation of caveolin-1 in FOXP3-overexpressed human gastric cancer cells

Pan

Gao

Zeng

et al. 2017

Sci Rep

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Forkhead box protein 3 (FOXP3) is implicated in tumor progression and prognosis in various types of tumor cells. We have recently reported that FOXP3 inhibited proliferation of gastric cancer (GC) cells through activating the apoptotic signaling pathway. In this study, we found that over-expression of FOXP3 inhibited GC cell migration, invasion and proliferation. Then, the label-free quantitative proteomic approach was employed to further investigating the down-stream proteins regulated by FOXP3, resulting in a total of 3,978 proteins quantified, including 186 significantly changed proteins. Caveolin-1 (CAV1), as a main constituent protein of caveolae, was one of those changed proteins up-regulated in FOXP3-overexpressed GC cells, moreover, it was assigned as one of the node proteins in the protein-protein interaction network and the key protein involved in focal adhesion pathway by bioinformatics analysis. Further biological experiments confirmed that FOXP3 directly bound to the promoter regions of CAV1 to positively regulate CAV1 transcription in GC cells. In summary, our study suggested that FOXP3 can be considered as a tumor suppressor in GC via positively regulating CAV1 through transcriptional activation, and this FOXP3-CAV1 transcriptional regulation axis may play an important role in inhibiting invasion and metastasis of GC cells. Data are available via ProteomeXchange under identifier PXD007725.

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Prognostic Value of Caveolin-1 Expression in Gastric Cancer: a Meta-analysis

Cited by 12 publications

References 16 publications

Caveolin‐1: An Oxidative Stress‐Related Target for Cancer Prevention

Caveolin‐1: An Oxidative Stress‐Related Target for Cancer Prevention

Silencing of caveolin-1 in fibroblasts as opposed to epithelial tumor cells results in increased tumor growth rate and chemoresistance in a human pancreatic cancer model

Quantitative proteomic Analysis Reveals up-regulation of caveolin-1 in FOXP3-overexpressed human gastric cancer cells

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