scaffolding protein; Forms a stable heterooligomeric complex with CAV2 that targets to lipid rafts and drives caveolae formation. Mediates the recruitment of CAVIN proteins (CAVIN1/2/3/4) to the caveolae. Interacts directly with G-protein alpha subunits and can functionally regulate their activity. Involved in the costimulatory signal essential for T-cell receptor (TCR)-mediated T-cell activation.
Tumorsuppressor
Caveolin-1 (CAV1) has significant roles in many primary tumors and metastasis, despite the fact that malignant cells from different cancer types have different profiles of CAV1 expression. CAV1 overexpression enhanced hepatocellular carcinoma cell invasiveness in vitro, and promoted tumorigenicity and lung metastasis in vivo. By contrast, CAV1 stable knockdown markedly reduced these malignant behaviors. Increased CAV-1 expression induces bladder cancer cell migration and promotes the epithelial-to-mesenchymal transition.
Due to its function in the negative regulation of signal transduction, loss of Cav1 has been implicated in the pathogenesis of many cancers. Cav1 overexpression decreases cell and tumor growth, whereas Cav1 knockdown increases these attributes in cutaneous squamous cell carcinoma cells. In addition, Cav1 knockdown increases the invasive ability and incidence of spontaneous lymph node metastasis. NIH 3T3 cells harboring antisense caveolin-1 exhibit anchorage-independent growth. NIH 3T3 cells harboring vector alone did not show foci formation or growth in soft agar. Three of the transformed cell lines were tumorigenic in immuno-deficient strains of mice, forming tumors with high frequency (65–100%). After 2–3 weeks, these tumors reached masses of ~2–4 g. Importantly, no tumors were observed with normal NIH 3T3 cells used for control injections.
Die ursächliche Beteiligung an der Entstehung von Tumoren als Onkogen ist nicht gezeigt.
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