Survival Promoting Activity of Caveolin1

Several studies using either overexpression or antisense suppression techniques demonstrated that caveolin-1 may act as a positive regulator of cell survival in certain cancer cells. This was first shown in mouse and human prostate cancer cells, where expression of caveolin-1 protects the cells from androgen deprivation-induced apoptosis and c-Myc-induced apoptosis, respectively [7,10]. In the former case, caveolin-1 was secreted from the cells, upon testosterone treatment, acting as an autocrine or paracrine pro-survival factor [9]. Similarly, overexpression of caveolin-1 in LNCaP human prostate cancer cells significantly reduced thapsigargin-induced apoptosis [12]. The pro-survival action of caveolin-1 in prostate cancer cells was recently confirmed in the TRAMP mouse model, where caveolin-1 gene knockout attenuated tumor progression and metastasis in vivo and stimulated apoptosis of tumor-derived cells both in vitro and in vivo [84]. We have recently shown that caveolin-1 expression in MCF-7 cells results in inhibition of anoikis

(detachment-induced apoptosis) [11] and of detachment-induced activation of p53 [13]. Interestingly, cellular resistance to anoikis was also recently shown to be caveolin-1-dependent in pancreatic adenocarcinoma cells [85]. Antisense inhibition of caveolin-1 expression sensitizes nonmalignant intestinal epithelial cells to anoikis [14]. Taken together, these data clearly indicate that caveolin-1 can promote cell survival upon environmental challenge in both normal and cancer cells.

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