BACKGROUND: Interleukin (IL)-6-mediated anti-apoptotic effects and drug-resistance mechanisms in prostate cancer cells were investigated. METHODS: IL-6 levels of PC-3 and LNCaP cells were studied by using ELISA. Protective effects of IL-6 on cytotoxic agent-induced apoptosis were studied by exogenous IL-6 in serum-starved PC-3 cells and by anti-sense IL-6 strategy. Western blotting and reverse transcription-polymerase chain reaction (RT-PCR) were used to determine IL-6 effects on Bcl-2 family proteins. Tetracycline-regulated Bcl-xL expression system and dominant negative STAT3 transfectants were used to study IL-6 signaling pathways and its anti-apoptosis effects. RESULTS: Exogenous IL-6 and anti-sense IL-6 oligonucleotide treatment conferred resistance to cytotoxic agent-induced apoptosis. Among Bcl-2 family proteins, only Bcl-xL was evidently increased by IL-6 stimulation. The anti-apoptotic effect of IL-6 can be significantly attenuated by anti-sense bcl-xL transfection and partially abrogated in dominant negative STAT3 transfectants. CONCLUSIONS: IL-6 is a survival factor against cytotoxic agent-induced apoptosis through both STAT3 and bcl-xL pathways in prostate cancer cells. Copyright 2004 Wiley-Liss, Inc.
BACKGROUND: Interleukin (IL)-6-mediated anti-apoptotic effects and drug-resistance mechanisms in prostate cancer cells were investigated. METHODS:IL-6 levels of PC-3 and LNCaP cells were studied by using ELISA. Protective effects of IL-6 on cytotoxic agent-induced apoptosis were studied by exogenous IL-6 in serum-starved PC-3 cells and by anti-sense IL-6 strategy. Western blotting and reverse transcription-polymerase chain reaction (RT-PCR) were used to determine IL-6 effects on Bcl-2 family proteins. Tetracycline-regulated Bcl-xL expression system and dominant negative STAT3 transfectants were used to study IL-6 signaling pathways and its anti-apoptosis effects. RESULTS: Exogenous IL-6 and anti-sense IL-6oligonucleotide treatment conferred resistance to cytotoxic agent-induced apoptosis. Among Bcl-2 family proteins, only Bcl-xL was evidently increased by IL-6 stimulation. The anti-apoptotic effect of IL-6 can be significantly attenuated by anti-sense bcl-xL transfection and partially abrogated in dominant negative STAT3 transfectants. CONCLUSIONS:IL-6 is a survival factor against cytotoxic agent-induced apoptosis through both STAT3 and bcl-xL pathways in prostate cancer cells. Copyright 2004 Wiley-Liss, Inc.
Authors: Jessica Bockhorn; Rachel Dalton; Chika Nwachukwu; Simo Huang; Aleix Prat; Kathy Yee; Ya-Fang Chang; Dezheng Huo; Yujia Wen; Kaitlin E Swanson; Tyler Qiu; Jun Lu; Seo Young Park; M Eileen Dolan; Charles M Perou; Olufunmilayo I Olopade; Michael F Clarke; Geoffrey L Greene; Huiping Liu Journal: Nat Commun Date: 2013 Impact factor: 14.919