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Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Oncotarget 2017 ; 8 (11): 17700-11 Nephropedia Template TP
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Capsazepine inhibits JAK/STAT3 signaling, tumor growth, and cell survival in prostate cancer #MMPMID27458171
Lee JH; Kim C; Baek SH; Ko JH; Lee SG; Yang WM; Um JY; Sethi G; Ahn KS
Oncotarget 2017[Mar]; 8 (11): 17700-11 PMID27458171show ga
Persistent STAT3 activation is seen in many tumor cells and promotes malignant transformation. Here, we investigated whether capsazepine (Capz), a synthetic analogue of capsaicin, exerts anticancer effects by inhibiting STAT3 activation in prostate cancer cells. Capz inhibited both constitutive and induced STAT3 activation in human prostate carcinoma cells. Capz also inhibited activation of the upstream kinases JAK1/2 and c-Src. The phosphatase inhibitor pervanadate reversed Capz-induced STAT3 inhibition, indicating that the effect of Capz depends on a protein tyrosine phosphatase. Capz treatment increased PTP? protein and mRNA levels. Moreover, siRNA-mediated knockdown of PTP? reversed the Capz-induced induction of PTP? and inhibition of STAT3 activation, indicating that PTP? is crucial for Capz-dependent STAT3 dephosphorylation. Capz also decreased levels of the protein products of various oncogenes, which in turn inhibited proliferation and invasion and induced apoptosis. Finally, intraperitoneal Capz administration decreased tumor growth in a xenograft mouse prostate cancer model and reduced p-STAT3 and Ki-67 expression. These data suggest that Capz is a novel pharmacological inhibitor of STAT3 activation with several anticancer effects in prostate cancer cells.