Shan Su1, Xueyan Lin2, Ning Ding3, Hong Zhang3, Qinghua Zhang3, Yumei Ding3, Xiaoman Hou2, Yongjie Tian4. 1. Department of Obstetrics and Gynecology, Provincial Hospital Affiliated to Shandong University, Shangdong, China; Department of Gynecology, The Central Hospital of Zibo, Shangdong, China. 2. Department of Obstetrics and Gynecology, Provincial Hospital Affiliated to Shandong University, Shangdong, China. 3. Department of Gynecology, The Central Hospital of Zibo, Shangdong, China. 4. Department of Obstetrics and Gynecology, Provincial Hospital Affiliated to Shandong University, Shangdong, China. Electronic address: tyjtyj64@163.com.
Abstract
BACKGROUND: To assess the effects of the poly (ADP-ribose) polymerase-1 (PARP-1) inhibitor PJ34 and ERK1/2 inhibitor U0126 on the proliferation and epithelial mesenchymal transitions (EMT) of cisplatin resistant ovarian cancer SKOV-3 cells. METHODS: Proliferation of SKOV-3 cells was evaluated using a 3-(4,5-dimethylthazol-2-yl)-2,5-diphenyl tetrazolium bromide assay with PJ34 and U0126 treatment. Expression changes of E-cadherin and vimentin with PJ34 and U0126 treatment was examined using Western blot and quantitative PCR. In addition, invasion assay was performed in cells treated with PJ34 and U0126. RESULTS: PJ34 and U0126 inhibited proliferation of SKOV-3 cells in a time dependent manner. PJ34 and U0126 suppressed the expression of vimentin and enhanced the expression of E-cadherin. PJ34 and U0126 reduced cell invasion. The inhibitory effects of PJ34 and U0126 were stronger than PJ34 alone. PJ34 inhibited the proliferation and invasion of SKOV-3 cells which can be enhanced by ERK1/2 inhibitor U0126. CONCLUSIONS: These inhibitory effects are partially due to PARP-1 and ERK1/2 mediated attenuation of EMT activity.
BACKGROUND: To assess the effects of the poly (ADP-ribose) polymerase-1 (PARP-1) inhibitor PJ34 and ERK1/2 inhibitor U0126 on the proliferation and epithelial mesenchymal transitions (EMT) of cisplatin resistant ovarian cancer SKOV-3 cells. METHODS: Proliferation of SKOV-3 cells was evaluated using a 3-(4,5-dimethylthazol-2-yl)-2,5-diphenyl tetrazolium bromide assay with PJ34 and U0126 treatment. Expression changes of E-cadherin and vimentin with PJ34 and U0126 treatment was examined using Western blot and quantitative PCR. In addition, invasion assay was performed in cells treated with PJ34 and U0126. RESULTS: PJ34 and U0126 inhibited proliferation of SKOV-3 cells in a time dependent manner. PJ34 and U0126 suppressed the expression of vimentin and enhanced the expression of E-cadherin. PJ34 and U0126 reduced cell invasion. The inhibitory effects of PJ34 and U0126 were stronger than PJ34 alone. PJ34 inhibited the proliferation and invasion of SKOV-3 cells which can be enhanced by ERK1/2 inhibitor U0126. CONCLUSIONS: These inhibitory effects are partially due to PARP-1 and ERK1/2 mediated attenuation of EMT activity.