Related Experiment Video
Updated: Nov 8, 2025
Generation of Prostate Cancer Cell Models of Resistance to the Anti-mitotic Agent Docetaxel
Published on: September 8, 2017
Propofol enhanced the cell sensitivity to paclitaxel (PTX) in prostatic cancer (PC) through modulation of HOTAIR
Xuesong Yang1,2, Jiao Qin3, Chunyu Gong4
1Department of Urology, Affiliated Hospital of North Sichuan Medical College, Nanchong, Sichuan, China.
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.
