Jian-Hua Guo1, Juan Zhou2, Yang Zhao2, Peng-Yue Liu2, Hai-Jun Yao2, Jun Da2, Ming Zhang2, Zhe Zhou2, Qi Chen2, Yu-Bing Peng2, Zhong Wang2. 1. Department of Urology and Andrology, Shanghai Ninth People's Hospital, Shanghai JiaoTong University School of Medicine Shanghai 200011, China ; Department of Urology, Shanghai Pudong Hospital, Fudan University Pudong Medical Centre Shanghai 201399, China. 2. Department of Urology and Andrology, Shanghai Ninth People's Hospital, Shanghai JiaoTong University School of Medicine Shanghai 200011, China.
Abstract
BACKGROUND: To investigated the peripheral stromal cell conditioned medium (CM) -stimulated c-kit-JAK2-STAT1 pathway in prostate cancer. METHODS: CM harvested from normal prostate peripheral stromal cells was added to DU145 cells. DU145 cell viability and migration were measured by cell counting kit-8 reagent and Transwell analysis respectively. Colony and sphere formation efficiencies of DU145 cells co-cultured with CM from human prostate stromal cells were also measured. DU145cells were stably transfected with lentivirus-mediated shRNA for c-kit silencing. RESULTS: C-kit expression in prostate cancer was found to be significantly higher than in benign prostatic hyperplasia and positively associated with Gleason scores. The growth, migration and capacity of clonogenic property of DU145 cells significantly increased upon exposure to peripheral stromal CM and then were inhibited after silencing the expression of c-kit. The levels of c-kit, pJAK2 and pSTAT1 were significantly induced by peripheral zone stromal CM compared with controls in serum free medium and the levels of pJAK2 and pSTAT1 decreased after c-kit silencing. CONCLUSIONS: C-kit hyper-expression promotes the development of prostate cancer. The peripheral stromal cell CM stimulated c-kit-JAK2-STAT1 pathway in prostate cancer cell viability, migration, and capacity of clonogenic property. This may lead to a greater understanding of the role of c-kit in prostate cancer and provide a potential therapeutic target for prostate cancer.
BACKGROUND: To investigated the peripheral stromal cell conditioned medium (CM) -stimulated c-kit-JAK2-STAT1 pathway in prostate cancer. METHODS: CM harvested from normal prostate peripheral stromal cells was added to DU145 cells. DU145 cell viability and migration were measured by cell counting kit-8 reagent and Transwell analysis respectively. Colony and sphere formation efficiencies of DU145 cells co-cultured with CM from human prostate stromal cells were also measured. DU145cells were stably transfected with lentivirus-mediated shRNA for c-kit silencing. RESULTS:C-kit expression in prostate cancer was found to be significantly higher than in benign prostatic hyperplasia and positively associated with Gleason scores. The growth, migration and capacity of clonogenic property of DU145 cells significantly increased upon exposure to peripheral stromal CM and then were inhibited after silencing the expression of c-kit. The levels of c-kit, pJAK2 and pSTAT1 were significantly induced by peripheral zone stromal CM compared with controls in serum free medium and the levels of pJAK2 and pSTAT1 decreased after c-kit silencing. CONCLUSIONS:C-kit hyper-expression promotes the development of prostate cancer. The peripheral stromal cell CM stimulated c-kit-JAK2-STAT1 pathway in prostate cancer cell viability, migration, and capacity of clonogenic property. This may lead to a greater understanding of the role of c-kit in prostate cancer and provide a potential therapeutic target for prostate cancer.
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