Caveolin-1 Is Associated with VCAM-1 Dependent Adhesion of Gastric Cancer Cells to Endothelial Cells

Shin, Jae-Young; Kim, Jongmin; Ryu, Byung–Kyu; Gil, Sung; Park, Heonyong

doi:10.1159/000094126

Cited by 36 publications

(24 citation statements)

References 38 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…It is interesting that K-Ras-mutated cell lines showed an elevated expression of caveolin-1 (Supplementary Figure S5d). Thus, we eliminated caveolin-1 through si-RNA (Shin et al, 2006) and measured p53 endocytosis. Si-caveolin-1 could block p53 endocytosis in A549 (Supplementary Figure S5e).…”

Section: Resultsmentioning

confidence: 99%

p53, secreted by K-Ras–Snail pathway, is endocytosed by K-Ras-mutated cells; implication of target-specific drug delivery and early diagnostic marker

Lee

Chung

et al. 2009

Oncogene

View full text Add to dashboard Cite

Section: Resultsmentioning

confidence: 99%

p53, secreted by K-Ras–Snail pathway, is endocytosed by K-Ras-mutated cells; implication of target-specific drug delivery and early diagnostic marker

Lee

Chung

et al. 2009

Oncogene

View full text Add to dashboard Cite

“…Primers were designed where possible to span intron/exon borders and specificity was checked using the European Molecular Biology Laboratory (EMBL)-GenBank database software using the BLAST program. The respective Forward and Reverse primers were: Targeted (siRNA) down-regulation of caveolin-1 and tamoxifen sensitivity assays As previously described [32,33] a siRNA duplex (21 nucleotides) targeting the caveolin-1 mRNA sequence 5 0 -AACCAGAAGGGACACACAGUU-3 0 was used to downregulate caveolin-1 protein expression and a siRNA duplex targeting the firefly luciferase (GL2) mRNA sequence 5 0 -AACGUACGCGGAAUACUUCGA-3 0 was used as a negative control. The duplexes were purchased from MWG (Ebersberg, Germany) as unprotected, desalted, and purified siRNA.…”

Section: Rt-pcrmentioning

confidence: 99%

Growth of hormone-dependent MCF-7 breast cancer cells is promoted by constitutive caveolin-1 whose expression is lost in an EGF-R-mediated manner during development of tamoxifen resistance

Thomas

Hutcheson

Campbell

et al. 2009

Breast Cancer Res Treat

View full text Add to dashboard Cite

Growth of hormone-dependent MCF-7 breast cancer cells is promoted by constitutive caveolin-1 whose expression is lost in an EGF-R-mediated manner during development of tamoxifen resistance. Breast Cancer Research and Treatment, Springer Verlag, 2009, 119 (3) Abstract Caveolin-1 displays both tumour-suppressor and tumour-promoter properties in breast cancer. Using characterised preclinical cell models for the transition of oestrogen-sensitive (WT-MCF-7 cells) to a tamoxifenresistant (TAM-R cells) phenotype we examined the role caveolin-1 in the development of hormone-resistant breast cancer. The WT-MCF-7 cells showed abundant expression of caveolin-1 which potentiated oestrogen-receptor (ERa) signalling and promoted cell growth despite caveolin-1 mediating inhibition of ERK signalling. In TAM-R cells caveolin-1 expression was negligible, repressed by EGF-R/ERK signalling. Pharmacological inhibition of EGFR/ERK in TAM-R cells restored caveolin-1 and also resulted in the emergence of pools of phosphorylated caveolin-1. WT-MCF-7 cells exposed to tamoxifen for upto 12 weeks displayed increased caveolin-1 (peaking by week 2) followed (after week 8) by a marked decrease as the cells progress to develop a stable tamoxifen-resistant phenotype. The targeted down-regulation (siRNA) of caveolin-1 in WT-MCF-7 cells reduced growth but did not affect their sensitivity to tamoxifen, suggesting loss of caveolin-1 alone is not sufficient to confer tamoxifen-resistance. Hyperactivation of EGFR/ERK is a feature of tamoxifen-resistant breast cancer cells, a principal driver of cell growth. Recombinant expression of caveolin-1 in TAM-R cells did not affect EGFR/ERK activity, potentially due to mislocalisation of caveolin-1 through hyperactivation of the mTOR pathway or altered caveolin-1 phosphorylation. This work defines a novel role for caveolin-1 with implications for the clinical course of breast cancer and identifies caveolin-1 as a potential drug target for the treatment of early oestrogen-dependent breast cancers. Further, the loss of caveolin-1 may have benefit as a molecular signature for tamoxifen resistance.

show abstract

“…It is also thought that enhanced Cav-2 expression alters signal transduction in UC, thus indicating a role for caveolae in IBD (5). Cav-1 is associated with VCAM-1 in progression of tumor vasculature and is necessary for remodeling the vasculature (138,167). Additionally, Sonveaux et al (142) showed that Cav1 Ϫ/Ϫ mouse cells exhibit poor tube formation in cultured endothelium (32).…”

Section: Angiogenic Mediators In Ibd and Experimental Colitismentioning

confidence: 99%

Pathogenic angiogenesis in IBD and experimental colitis: new ideas and therapeutic avenues

Chidlow

Shukla²,

Grisham³

et al. 2007

American Journal of Physiology-Gastrointestinal and Liver Physi

144

114

View full text Add to dashboard Cite

Chidlow JH Jr, Shukla D, Grisham MB, Kevil CG. Pathogenic angiogenesis in IBD and experimental colitis: new ideas and therapeutic avenues. Am J Physiol Gastrointest Liver Physiol 293: G5-G18, 2007. First published April 26, 2007; doi:10.1152/ajpgi.00107.2007.-Angiogenesis is now understood to play a major role in the pathology of chronic inflammatory diseases and is indicated to exacerbate disease pathology. Recent evidence shows that angiogenesis is crucial during inflammatory bowel disease (IBD) and in experimental models of colitis. Examination of the relationship between angiogenesis and inflammation in experimental colitis shows that initiating factors for these responses simultaneously increase as disease progresses and correlate in magnitude. Recent studies show that inhibition of the inflammatory response attenuates angiogenesis to a similar degree and, importantly, that inhibition of angiogenesis does the same to inflammation. Recent data provide evidence that differential regulation of the angiogenic mediators involved in IBD-associated chronic inflammation is the root of this pathological angiogenesis. Many factors are involved in this phenomenon, including growth factors/cytokines, chemokines, adhesion molecules, integrins, matrix-associated molecules, and signaling targets. These factors are produced by various vascular, inflammatory, and immune cell types that are involved in IBD pathology. Moreover, recent studies provide evidence that antiangiogenic therapy is a novel and effective approach for IBD treatment. Here we review the role of pathological angiogenesis during IBD and experimental colitis and discuss the therapeutic avenues this recent knowledge has revealed. inflammation; T cells; growth factors; adhesion molecules; antiangiogenesis ANGIOGENESIS PLAYS AN IMPORTANT role in many chronic inflammatory diseases including but not limited to diabetic retinopathy, atherosclerosis, rheumatoid arthritis, hypercholesterolemia, and psoriasis. It has been suggested that the angiogenic components of these diseases contribute to and exacerbate disease conditions (26, 31). Recent findings, both clinical and experimental, indicate that angiogenesis also plays a crucial role in the inflammatory bowel diseases (IBD), consisting of Crohn's disease (CD) and ulcerative colitis (UC) (31,37,58,131,155). Development of new vasculature during chronic inflammation may play a negative "pathological" role by contributing to increased inflammatory responses due to dysfunctional new vessel architecture and increases in the recruitment of inflammatory cell types. Importantly, recent data have shown that angiogenic inhibition during chronic inflammatory diseases attenuates further inflammation and disease pathology (31, 37, 51). As such, expanding our knowledge of how pathological angiogenesis occurs during IBD will further our ability to treat patients with these diseases. IBD PathogenesisCD and UC are idiopathic inflammatory disorders of the intestine and/or colon in which patients suffer from rectal bleeding, severe...

show abstract

Caveolin-1 Is Associated with VCAM-1 Dependent Adhesion of Gastric Cancer Cells to Endothelial Cells

Cited by 36 publications

References 38 publications

p53, secreted by K-Ras–Snail pathway, is endocytosed by K-Ras-mutated cells; implication of target-specific drug delivery and early diagnostic marker

p53, secreted by K-Ras–Snail pathway, is endocytosed by K-Ras-mutated cells; implication of target-specific drug delivery and early diagnostic marker

Growth of hormone-dependent MCF-7 breast cancer cells is promoted by constitutive caveolin-1 whose expression is lost in an EGF-R-mediated manner during development of tamoxifen resistance

Pathogenic angiogenesis in IBD and experimental colitis: new ideas and therapeutic avenues

Contact Info

Product

Resources

About