Xuesong Yang1,2, Jiao Qin3, Chunyu Gong4, Jing Yang5. 1. Department of Urology, Affiliated Hospital of North Sichuan Medical College, Nanchong, Sichuan, China. 2. Department of Urology, The First Affiliated Hospital of Jinan University, Guangzhou, China. 3. Department of Anesthesiology, Affiliated Hospital of North Sichuan Medical College, Nanchong, Sichuan, China. 4. Department of Urology , West China Fourth Hospital, Sichuan University, Chengdu, Sichuan, China. grd89562@126.com. 5. Department of Anesthesiology, West China Hospital, Sichuan University, No. 38, Guoxue Ave, Wuhou, Chengdu, Sichuan, 610041, China. hce85525@126.com.
Abstract
BACKGROUND: PTX is widely used in cancer treatments. OBJECTIVE: In this paper, we explored the role and potential molecular mechanism of propofol in regulating PTX sensitivity in PC cells. METHODS: Prostatic cancer cell line PC3 was treated using different concentrations of PTX (10 nM, 50 nM), propofol (150 μM, 300 μM) or transfected with overexpressed HOTAIR plasmid. HOTAIR expression was analyzed by RT-qPCR. Apoptosis of PC3 cells was observed by flow cytometry method while cell viability was evaluated by CCK-8. Moreover, apoptosis-related genes, Bcl-2 and Bax were detected by Western blot methods. E-cadherin, N-cadherin and Vimentin protein concentrations were monitored by ELISA. RESULTS: PTX significantly increased apoptosis of PC3 cells and reduced cell viability in a dose-dependent manner. Moreover, Protein expression of Bcl-2 was obviously inhibited while Bax protein expression level was provoked. Furthermore, E-cadherin protein concentration increased while N-cadherin and Vimentin decreased due to increasing PTX treatments. HOTAIR expression dropped due to PTX treatment while overexpression of HOTAIR induced cell viability, EMT and deterred apoptosis. Propofol ignited the PTX function while upregulation of HOTAIR partially reversed this. CONCLUSION: Propofol enhanced paclitaxel sensitivity in prostatic cancer cells through modulation of HOTAIR in vitro.
BACKGROUND: PTX is widely used in cancer treatments. OBJECTIVE: In this paper, we explored the role and potential molecular mechanism of propofol in regulating PTX sensitivity in PC cells. METHODS: Prostatic cancer cell line PC3 was treated using different concentrations of PTX (10 nM, 50 nM), propofol (150 μM, 300 μM) or transfected with overexpressed HOTAIR plasmid. HOTAIR expression was analyzed by RT-qPCR. Apoptosis of PC3 cells was observed by flow cytometry method while cell viability was evaluated by CCK-8. Moreover, apoptosis-related genes, Bcl-2 and Bax were detected by Western blot methods. E-cadherin, N-cadherin and Vimentin protein concentrations were monitored by ELISA. RESULTS: PTX significantly increased apoptosis of PC3 cells and reduced cell viability in a dose-dependent manner. Moreover, Protein expression of Bcl-2 was obviously inhibited while Bax protein expression level was provoked. Furthermore, E-cadherin protein concentration increased while N-cadherin and Vimentin decreased due to increasing PTX treatments. HOTAIR expression dropped due to PTX treatment while overexpression of HOTAIR induced cell viability, EMT and deterred apoptosis. Propofol ignited the PTX function while upregulation of HOTAIR partially reversed this. CONCLUSION: Propofol enhanced paclitaxel sensitivity in prostatic cancer cells through modulation of HOTAIR in vitro.
Entities:
Keywords:
HOTAIR; Paclitaxel; Propofol; Prostate cancer