Impact of NF-kappaB inhibitor on STAT3 translocation in PC-3 prostate cancer cell line.
- Author:
Chun-Yan LI
1
;
Hua-Xin ZHAO
;
Xi ZHANG
;
Li CHU
;
Jue-Min FANG
;
Hui HAN
;
Xi LIU
;
Qing XU
Author Information
- Publication Type:Journal Article
- MeSH: Caffeic Acids; pharmacology; Cell Line, Tumor; Humans; Interleukin-6; metabolism; pharmacology; Male; NF-kappa B; antagonists & inhibitors; Phenylethyl Alcohol; analogs & derivatives; pharmacology; Prostatic Neoplasms; metabolism; STAT3 Transcription Factor; metabolism; Signal Transduction; drug effects; Tumor Necrosis Factor-alpha; pharmacology
- From: National Journal of Andrology 2013;19(6):487-494
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo observe the changes in the expressions of STAT3 and NF-KB in PC-3 cells after IL-6 stimulation and to verify the effects of the NF-KB inhibitor caffeic acid phenethyl ester (CAPE) on the expressions of p-STAT3 and IL-6 in the PC-3 prostate cancer cell line.
METHODSPC-3 prostate cancer cells were treated with IL-6 at 20 ng/ml for 5, 10, 20, 30 and 45 min. The protein and mRNA expressions of STAT3 and NF-kappaB were measured by Western blot and real time PCR, respectively, and the cell cycle was detected by flow cytometry. The PC-3 cells were exposed to TNF-alpha or TNF-alpha + CAPE, followed by determination of the IL-6 expression in the supernatant of the cells by ELISA and the expression of p-STAT3 by Western blot.
RESULTSAfter IL-6 stimulation, both the expression of p-STAT3 protein and the proliferation index of the PC-3 cells were significantly increased, and so were the expressions of IL-6 and p-STAT3 protein in the supernatant after TNF-alpha treatment (P < 0.05). TNF-alpha + CAPE induced statistically lower expressions of IL-6 and p-STAT3 than TNF-alpha alone (P < 0.05).
CONCLUSIONCAPE can inhibit IL-6 secretion induced by TNF-alpha in PC-3 cells and thus suppress STAT3 translocation. Therefore, by inhibiting the expression of NF-kappaB and affecting STAT3 and other related cell signaling pathways, CAPE may become a new therapeutic option for prostate cancer.