Tyrosine-317 of p52Shc mediates androgen-stimulated proliferation signals in human prostate cancer cells

VEGF–integrin interplay controls tumor growth and vascularization

“…We found that ␣v␤3 integrin clustering leads to p66 Shc phosphorylation, which was a necessary event for ␣v␤3-mediated VEGF expression. The association of Shc, primarily of the p46 and p52 isoforms, with integrins has been reported in several studies (28)(29)(30). Our results suggest that Shc recruitment is not sufficient for ␣v␤3-mediated effects on VEGF production but that Shc phosphorylation (activation) may be required.…”

Expression of p66Shc protein correlates with proliferation of human prostate cancer cells

“…The doubling time of each cell line has been given as a measure of their growth rates ( a Navone et al, 1997; b Horoszewicz et al, 1983; Kaighn et al, 1979; d Iizumi et al, 1987; e Stone et al, 1978) p66 Shc protein in human prostate cancer cell proliferation S Veeramani et al C-51 and C-33 cells, whereas p52 Shc protein level was approximately similar in all cells (Figure 2a, inner panel). Since Shc family members are tyrosine phosphorylated in mediating the growth signals from tyrosine phosphorylated receptor tyrosine kinases (Ravichandran, 2001;Lee et al, 2004b) Lee et al, 2004b). Similar negative results were obtained by using the antibody against pY239 or pY317 of p52 Shc that could also react with the corresponding sites in p66…”

“…Shc protein with the total cell lysate proteins (Lee et al, 2004b). Nevertheless, cPAcP was highly expressed in C-33 cells, while it was only barely detected in C-81 cells, thus, inversely correlating with their relative p66 Shc protein levels ( Figure 2a, inner panel).…”

“…We used EGF and 5a-dihydrotestosterone (DHT), which could upregulate the proliferation of LNCaP C-33 cells and downregulate the cPAcP (Lin et al, 1992Meng and Lin, 1998;Lee et al, 2004b), and examined their effects on the protein levels of p66 Shc in those cells. As shown in Figure 3a, p66…”

TRIM31 interacts with p52Shc and inhibits Src-induced anchorage-independent growth

“…p52 Shc is also responsible for transducing anchorage-dependent growth signaling and may be involved in the adhesion process and metastasis of cancer cells [24,30,31].…”