Caveolin-1 expression is associated with high-grade bladder cancer

Rajjayabun, P.; Garg, Saumil; Durkan, Garrett; Charlton, Richard; Robinson, Mary C.; Mellon, J. Kilian

doi:10.1016/s0090-4295(01)01337-1

Cited by 105 publications

(75 citation statements)

References 20 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…52 Caveolin-1 expression is correlated with tumor stage and grade of bladder transitional cell carcinoma (TCC). 53,54 Caveolin-1 expression was correlated significantly with T stage and grade of bladder TCC, which strongly indicates that caveolin-1 is involved in tumor progression and that the increased expression of caveolin-1 is a late event in urothelial carcinomas. 55 The increased expression of caveolin-1 is associated with tumor progression and poor prognosis in Figure 11.…”

Section: Discussionmentioning

confidence: 84%

Transcriptional Repression of Caveolin-1 (CAV1) Gene Expression by GATA-6 in Bladder Smooth Muscle Hypertrophy in Mice and Human Beings

Boopathi

Gomes

Goldfarb

et al. 2011

The American Journal of Pathology

View full text Add to dashboard Cite

Hypertrophy occurs in urinary bladder wall smooth muscle (BSM) in men with partial bladder outlet obstruction (PBOO) caused by benign prostatic hyperplasia (BPH) and in animal models of PBOO. Hypertrophied BSM from the rabbit model exhibits downregulation of caveolin-1, a structural and functional protein of caveolae that function as signaling platforms to mediate interaction between receptor proteins and adaptor and effector molecules to regulate signal generation, amplification, and diversification. Caveolin-1 expression is diminished in PBOO-induced BSM hypertrophy in mice and in men with BPH. The proximal promoter of the human and mouse caveolin-1 (CAV1) gene was characterized, and it was observed that the transcription factor GATA-6 binds this promoter, causing reduced expression of caveolin-1. Furthermore, caveolin-1 expression levels inversely correlate with the abundance of GATA-6 in BSM hypertrophy in mice and human beings. Benign prostatic hyperplasia (BPH) is common in aging men and is often associated with lower urinary tract symptoms. Partial bladder outlet obstruction (PBOO) has long been considered a key factor in the mechanism through which BPH causes lower urinary tract symptoms. PBOO-induced lower urinary tract symptoms are associated with bladder wall smooth muscle (BSM) remodeling including hypertrophy, thereby altering bladder contractility.

show abstract

Section: Discussionmentioning

confidence: 84%

Transcriptional Repression of Caveolin-1 (CAV1) Gene Expression by GATA-6 in Bladder Smooth Muscle Hypertrophy in Mice and Human Beings

Boopathi

Gomes

Goldfarb

et al. 2011

The American Journal of Pathology

View full text Add to dashboard Cite

show abstract

“…21,25,26 Previously, we and others found that expression of caveolin-1 (cav-1), the major component of caveolae, is elevated in prostate cancer and other malignancies. [27][28][29][30][31][32][33][34][35][36][37][38][39][40] To address the molecular mechanism of cav-1-mediated cell survival, we explored a possible link between cav-1 overexpression and Akt activation in prostate cancer cells. When we compared PI3-K-Akt signaling activities in cav-1-expressing LNCaP cells that had undergone adenoviral vector-mediated cav-1 gene transduction with PI3-K-Akt signaling activities in cav-1-negative vector control LNCaP cells, we found that Akt, but not PI3-K activities, were significantly higher in the former.…”

Section: Mechanisms Of Akt Regulationmentioning

confidence: 99%

The emerging role of the PI3-K-Akt pathway in prostate cancer progression

Ittmann

Ayala

et al. 2005

Prostate Cancer Prostatic Dis

112

View full text Add to dashboard Cite

The PI3-K-Akt pathway plays a central role in the development and progression of prostate cancer and other malignancies. We review original studies and summarize relevant sections of previous reviews concerning the relationships between abnormalities in the PI3-K-Akt pathway and prostate cancer progression. We discuss laboratory and clinical data that indicate gene perturbation and dysregulation of PI3-K-Akt pathway is common in prostate cancer and other malignancies. We further discuss the critical role of the PI3-K-Akt pathway in the oncogenic signaling network and provide examples that establish the PI3-K-Akt pathway as a focal point for the future development of informative biomarkers and effective therapies for prostate cancer.

show abstract

“…Caveolin-1 was first thought to have tumour suppressor properties (Razani et al, 2001a, b;Hnasko and Lisanti, 2003), based on the finding of an arguable inactivating point mutation in CAV1, the silencing of CAV1 gene expression by promoter hypermethylation in breast cell lines and prostate tumour samples (Engelman et al, 1999;Hurlstone et al, 1999;Cui et al, 2001) and the apparent downregulation of CAV1 in breast cancer (Chen et al, 2004;Park et al, 2005). In recent years, there has been increasingly more coherent data to suggest that CAV1 and CAV2 may also have oncogenic properties in breast (Hurlstone et al, 1999;Pinilla et al, 2006; Van den Eynden et al, 2006;Savage et al, 2007Savage et al, , 2008, prostate (Yang et al, 1998;Thompson et al, 1999), bladder (Rajjayabun et al, 2001;Fong et al, 2003), oesophageal (Kato et al, 2002;Ando et al, 2007), thyroid, pancreatic, non-small cell and squamous lung cancer (Kato et al, 2004;Sunaga et al, 2004).…”

mentioning

confidence: 99%

Caveolin 1 and Caveolin 2 are associated with breast cancer basal-like and triple-negative immunophenotype

et al. 2008

View full text Add to dashboard Cite

Caveolin-1 (CAV1) and caveolin 2 (CAV2) are the principal structural proteins of caveolae, sphingolipid and cholesterol-rich invaginations of the plasma membrane involved in vesicular trafficking and signal transduction. Over the recent years there has been controversy about their role in breast cancer and their suitability as markers of basal-like phenotype. Caveolin-1 and CAV2 protein expression was assessed on a tissue microarray containing 880 unselected invasive breast cancer cases, by means of immunohistochemistry. Caveolin-1 and CAV2 expression was observed in 13.4 and 5.9% of all breast cancer, respectively. Their expression was strongly associated with high histological grade, lack of steroid hormone receptor positivity (ER and PR), and expression of basal markers (basal cytokeratins, P63, P-cadherin). Furthermore, there was a significant association between CAV1 and CAV2 expression and basal-like phenotype. On univariate analysis only CAV2 had a prognostic impact on breast cancer-specific survival; however, this was not independent from other traditional markers on multivariate analysis. Our results demonstrate that both CAV1 and CAV2 are associated with basal-like phenotype. Further studies are warranted to determine whether they play an oncogenic role in basal-like/triple-negative breast cancer development or are just surrogate markers for this subgroup.

show abstract

Caveolin-1 expression is associated with high-grade bladder cancer

Cited by 105 publications

References 20 publications

Transcriptional Repression of Caveolin-1 (CAV1) Gene Expression by GATA-6 in Bladder Smooth Muscle Hypertrophy in Mice and Human Beings

Transcriptional Repression of Caveolin-1 (CAV1) Gene Expression by GATA-6 in Bladder Smooth Muscle Hypertrophy in Mice and Human Beings

The emerging role of the PI3-K-Akt pathway in prostate cancer progression

Caveolin 1 and Caveolin 2 are associated with breast cancer basal-like and triple-negative immunophenotype

Contact Info

Product

Resources

About