Caveolin-1 Regulates Endothelial Adhesion of Lung Cancer Cells via Reactive Oxygen Species-Dependent Mechanism

Chanvorachote, Pithi; Chunhacha, Preedakorn

doi:10.1371/journal.pone.0057466

Cited by 29 publications

(17 citation statements)

References 28 publications

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“…Multiple independent studies have indicated that CAV1 has a tumor-suppressor role in lung cancer and other types of malignancy (22,23,(31)(32)(33), which is consistent with the current findings, which revealed that the expression of CAV1 was significantly attenuated in lung cancer patients compared with healthy individuals. With regard to the mechanism, studies have demonstrated that CAV1 suppresses vascular cell adhesion protein 1-mediated adhesion between human lung cancer cells and endothelial cells by attenuating the production of hydrogen peroxide and hydroxyl radicals (32). In addition, CAV1 interacts with the StAR-related lipid transfer domain of deleted in liver cancer 1, another tumor suppressor that is frequently mutated in non-small cell lung cancer patients, and forms a complex to inhibit cancer cell migration and neoplastic development (31).…”

Section: Discussionsupporting

confidence: 92%

Pathogenic mechanisms of lung adenocarcinoma in smokers and non-smokers determined by gene expression interrogation

Chen

2015

Oncology Letters

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Abstract. Cigarette smoking is the leading risk factor for lung cancer, which accounts for the highest number of cancer-related mortalities worldwide in men and women. Individuals with a history of smoking are 15-30 times more likely to develop lung cancer compared with those who do not smoke. However, our understanding of the underlying molecular mechanisms that contribute to lung tumorigenesis in smokers versus non-smokers remains incomplete. In order to investigate such mechanisms, the present study aimed to systemically interrogate microarray datasets from tumor biopsies and matching normal tissues from stage I and II lung adenocarcinoma patients who had never smoked or were current smokers. The gene expression analysis identified 422 (99 upregulated and 323 downregulated) and 534 (174 upregulated and 360 downregulated) differentially-expressed genes from the never-smokers and current smokers, respectively, and the two groups shared 277 genes that exhibited similar trends of alteration. These genes encode regulators that are involved in a variety of cellular functions, including collagen metabolism and homeostasis of caveolae plasma membranes. Gene Ontology and Kyoto Encyclopedia of Genes and Genomes characterization indicated that biological pathways, including extracellular matrix-receptor interaction and cell migration and proliferation, were all affected in the lung cancer patients regardless of the smoking status. However, smoking induced a unique gene expression pattern characterized by upregulation of cell cycle regulators (CDK1, CCNB1 and CDC20), as well as significantly affected biological networks, including p53 signaling pathways. Taken together, these findings suggest novel mechanistic insights, and provide an improved understanding of the smoking-induced molecular alterations that contribute to the pathogenesis of lung adenocarcinoma.

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Section: Discussionsupporting

confidence: 92%

Pathogenic mechanisms of lung adenocarcinoma in smokers and non-smokers determined by gene expression interrogation

Chen

2015

Oncology Letters

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“…Shiroto et al showed that mitochondrial ROS production was increased in endothelial cells after cav-1 knockdown, and their results established that cav-1 plays a key role in regulating oxidative stress in the endothelium and may represent a critical target in cardiovascular diseases [40] . Chanvorachote and Chunhacha showed that cav-1 regulates the endothelial adhesion of lung cancer cells via a ROS-dependent mechanism [41] . Phosphorylation of cav-1 at tyrosine 14 was first identified in v-Src-transformed cells and facilitated the cav-1 interaction with other proteins in a stimulus-specific fashion [17] .…”

Section: Discussionmentioning

confidence: 99%

Curcumin attenuates high glucose-induced podocyte apoptosis by regulating functional connections between caveolin-1 phosphorylation and ROS

et al. 2016

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Aim: Caveolin-1 (cav-1) is a major multifunctional scaffolding protein of caveolae. Cav-1 is primarily expressed in mesangial cells, renal proximal tubule cells and podocytes in kidneys. Recent evidence shows that the functional connections between cav-1 and ROS play a key role in many diseases. In this study we investigated whether regulating the functional connections between cav-1 and ROS in kidneys contributed to the beneficial effects of curcumin in treating diabetic nephropathy in vitro and in vivo. Methods: Cultured mouse podocytes (mpc5) were incubated in a high glucose (HG, 30 mmol/L) medium for 24, 48 or 72 h. Male rats were injected with STZ (60 mg/kg, ip) to induce diabetes. ROS generation, SOD activity, MDA content and caspase-3 activity in the cultured cells and kidney cortex homogenate were determined. Apoptotic proteins and cav-1 phosphorylation were analyzed using Western blot analyses. Results: Incubation in HG-containing medium time-dependently increased ROS production, oxidative stress, apoptosis, and cav-1 phosphorylation in podocytes. Pretreatment with curcumin (1, 5, and 10 μmol/L) dose-dependently attenuated these abnormalities in HG-treated podocytes. Furthermore, in HG-containing medium, the podocytes transfected with a recombinant plasmid GFP-cav-1 Y14F (mutation at a cav-1 phosphorylation site) exhibited significantly decreased ROS production and apoptosis compared with the cells transfected with empty vector. In diabetic rats, administration of curcumin (100 or 200 mg/kg body weight per day, ig, for 8 weeks) not only significantly improved the renal function, but also suppressed ROS levels, oxidative stress, apoptosis and cav-1 phosphorylation in the kidneys. Conclusion: Curcumin attenuates high glucose-induced podocyte apoptosis in vitro and diabetic nephropathy in vivo partly through regulating the functional connections between cav-1 phosphorylation and ROS.

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“…Others identified further potential target molecules responsible for an upregulation of VCAM‐1 contributing to cancer metastasis e.g . heparanase, caveolin, and IL‐8 . A downregulation approach for VCAM‐1 expressed by TCs or LEC is currently not available.…”

Section: Structural and Functional Aspects Of Vcam‐1 Biologymentioning

confidence: 99%

“…heparanase, caveolin, and IL-8. 105,161,162 A downregulation approach for VCAM-1 expressed by TCs or LEC is currently not available.…”

Section: Vcam-1 As Biomarker and As Potential Therapeutic Targetmentioning

confidence: 99%

Vascular cell adhesion molecule‐1 (VCAM‐1)—An increasing insight into its role in tumorigenicity and metastasis

Schlesinger

Bendas

2014

Intl Journal of Cancer

193

148

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Vascular cell adhesion molecule-1 (VCAM-1) first attracted attention more than two decades ago as endothelial adhesion receptor with key function for leukocyte recruitment in term of cellular immune response. The early finding of VCAM-1 binding to melanoma cells, and thus a suggested mechanistic contribution to metastatic spread, was the first and for a long time the only link of VCAM-1 to cancer sciences. In the last few years, hallmarked by a growing insight into the molecular understanding of tumorigenicity and metastasis, an impressive variety of VCAM-1 functionalities in cancer have been elucidated. The present review aims to provide a current overview of VCAM-1 relevance for tumor growth, metastasis, angiogenesis, and related processes. By illustrating the intriguing role of VCAM-1 in cancer disease, VCAM-1 is suggested as a new and up to now underestimated target in cancer treatment and in clinical diagnosis of malignancies.Structural and functional aspects of VCAM-1 biology VCAM-1 (CD106) was discovered independently by two groups in 1989. First named INCAM-110 due to the TNF-a or IL-1 "inducibility" on HUVEC cells, it was later termed VCAM-1 when its ability to mediate a firm melanoma cell adhesion was revealed.

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Caveolin-1 Regulates Endothelial Adhesion of Lung Cancer Cells via Reactive Oxygen Species-Dependent Mechanism

Cited by 29 publications

References 28 publications

Pathogenic mechanisms of lung adenocarcinoma in smokers and non-smokers determined by gene expression interrogation

Pathogenic mechanisms of lung adenocarcinoma in smokers and non-smokers determined by gene expression interrogation

Curcumin attenuates high glucose-induced podocyte apoptosis by regulating functional connections between caveolin-1 phosphorylation and ROS

Vascular cell adhesion molecule‐1 (VCAM‐1)—An increasing insight into its role in tumorigenicity and metastasis

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