Overexpression of caveolin‐1 in esophageal squamous cell carcinoma correlates with lymph node metastasis and pathologic stage

Kato, Keizo; Hida, Yasuhiro; Miyamoto, Masaki; Hashida, Hideaki; Shinohara, Toshiya; Itoh, Tomoo; Okushiba, Shunichi; Kondo, Satoshi; Katoh, Hiroyuki

doi:10.1002/cncr.10329.abs

Cited by 14 publications

(15 citation statements)

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“…How might the overexpression of Cav-1 and caveolae contribute to the hyperproliferative phenotype of IPAH? Certain neoplasms [i.e., prostate cancer (39,40), bladder cancer (41), adenocarcinomas (42), esophageal squamous cell carcinomas (43), and both benign and malignant smooth muscle tumors (44)] have elevated Cav-1 expression. Timme et al have shown an interplay between Cav-1 and c-Myc-induced apoptosis: the Cav-1 gene can be down-regulated by c-myc, and maintaining high levels of Cav-1 suppresses c-myc-induced apoptosis (45).…”

Section: Discussionmentioning

confidence: 99%

Increased smooth muscle cell expression of caveolin‐1 and caveolae contribute to the pathophysiology of idiopathic pulmonary arterial hypertension

et al. 2007

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Vasoconstriction and vascular medial hypertrophy, resulting from increased intracellular [Ca2+] in pulmonary artery smooth muscle cells (PASMC), contribute to elevated vascular resistance in patients with idiopathic pulmonary arterial hypertension (IPAH). Caveolae, microdomains within the plasma membrane, contain the protein caveolin, which binds certain signaling molecules. We tested the hypothesis that PASMC from IPAH patients express more caveolin-1 (Cav-1) and caveolae, which contribute to increased capacitative Ca2+ entry (CCE) and DNA synthesis. Immunohistochemistry showed increased expression of Cav-1 in smooth muscle cells but not endothelial cells of pulmonary arteries from patients with IPAH. Subcellular fractionation and electron microscopy confirmed the increase in Cav-1 and caveolae expression in IPAH-PASMC. Treatment of IPAH-PASMC with agents that deplete membrane cholesterol (methyl-beta-cyclodextrin or lovastatin) disrupted caveolae, attenuated CCE, and inhibited DNA synthesis of IPAH-PASMC. Increasing Cav-1 expression of normal PASMC with a Cav-1-encoding adenovirus increased caveolae formation, CCE, and DNA synthesis; treatment of IPAH-PASMC with siRNA targeted to Cav-1 produced the opposite effects. Treatments that down-regulate caveolin/caveolae expression, including cholesterol-lowering drugs, reversed the increased CCE and DNA synthesis in IPAH-PASMC. Increased caveolin and caveolae expression thus contribute to IPAH-PASMC pathophysiology. The close relationship between caveolin/caveolae expression and altered cell physiology in IPAH contrast with previous results obtained in various animal models, including caveolin-knockout mice, thus emphasizing unique features of the human disease. The results imply that disruption of caveolae in PASMC may provide a novel therapeutic approach to attenuate disease manifestations of IPAH.

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Section: Discussionmentioning

confidence: 99%

Increased smooth muscle cell expression of caveolin‐1 and caveolae contribute to the pathophysiology of idiopathic pulmonary arterial hypertension

et al. 2007

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“…Caveolin 1 apparently plays a tumour suppressive function by virtue of its caveolin scaffolding domain (residues 82-101), which binds and inhibits several pro-oncogenic signalling molecules, such as SFK and MAP kinases. On the other hand, caveolin 1 has been defined as a prognostic marker for aggressive prostate, pancreatic and esophageal carcinoma, and an important mediator of hormone-dependent signal transduction [40][41][42]. In prostate cancer, the progression of malignancy has been shown to directly correlate with caveolin 1 expression levels [43], and caveolin ) transfected cells were subjected to Western blotting and probed with anti-caveolin antibody to detect endogenous and exogenously expressed caveolins and anti-GAPDH as a loading control.…”

Section: Discussionmentioning

confidence: 99%

Invadopodia biogenesis is regulated by caveolin‐mediated modulation of membrane cholesterol levels

Caldieri

Giacchetti

Beznoussenko

et al. 2008

J Cellular Molecular Medi

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Introduction Invasive tumoural or transformed cells grown on an extracellular matrix (ECM) substratum extend proteolytically active protrusions into the matrix from their ventral surfaces; these protrusions have been termed invadopodia [1]. Invadopodial protrusions are actin-based structures enriched in integrins Abstract Invadopodia are proteolytically active protrusions formed by invasive tumoural cells when grown on an extracellular matrix (ECM) substratum. Clearly, invadopodia are specialized membrane domains acting as sites of signal transduction and polarized delivery of components required for focalized ECM degradation. For these reasons, invadopodia are a model to study focal ECM degradation by tumour cells. We investigated the features of invadopodia membrane domains and how altering their composition would affect invadopodia biogenesis and function. This was achieved through multiple approaches including manipulation of the levels of cholesterol and other lipids at the plasma membrane, alteration of cholesterol trafficking by acting on caveolin 1 expression and phosphorylation. We show that cholesterol depletion impairs invadopodia formation and persistence, and that invadopodia themselves

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“…105 In recent years, increasing evidence demonstrates that Cav1 is suppressed at the early stages of transformation and carcinogenesis, but upregulated and associated with cancer progression, metastasis and poor prognosis in later stages of various carcinomas. [106][107][108][109] Cav1 is not detectable in non-neoplastic livers, but HCC (26%) show increased expression. 110 In mouse HCC cell lines, cells with higher invasive ability have strong Cav1 expression.…”

Section: Caveolin-1 (Cav1)mentioning

confidence: 98%

Role and significance of focal adhesion proteins in hepatocellular carcinoma

Yam

Tse

2009

J of Gastro and Hepatol

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Focal adhesions are structural links between the extracellular matrix and actin cytoskeleton. They are important sites where dynamic alterations of proteins in the focal contacts are involved during cell movement. Focal adhesions are composed of diverse molecules, for instance, receptors, structural proteins, adaptors, GTPase, kinases and phosphatases. These molecules play critical roles in normal physiological events such as cellular adhesion, movement, cytoskeletal structure and intracellular signaling pathways. In cancers, aberrant expression and altered functions of focal adhesion proteins contribute to adverse tumor behavior. It is evident that these proteins do not function alone, but rather associate and work together in the process of tumor development and cancer metastasis. Focal adhesion proteins have been shown to play critical roles in hepatocellular carcinoma. Understanding the molecular interactions and mechanisms of the interconnected focal adhesion proteins is of particular importance in understanding mechanisms underlying hepatocellular carcinoma progression and development of potential effective treatment.

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Overexpression of caveolin‐1 in esophageal squamous cell carcinoma correlates with lymph node metastasis and pathologic stage

Abstract: Over-expression of caveolin-1 is associated with lymph node metastasis and a worse prognosis after surgery in esophageal squamous cell carcinoma.

Cited by 14 publications

References 0 publications

Increased smooth muscle cell expression of caveolin‐1 and caveolae contribute to the pathophysiology of idiopathic pulmonary arterial hypertension

Increased smooth muscle cell expression of caveolin‐1 and caveolae contribute to the pathophysiology of idiopathic pulmonary arterial hypertension

Invadopodia biogenesis is regulated by caveolin‐mediated modulation of membrane cholesterol levels

Role and significance of focal adhesion proteins in hepatocellular carcinoma

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