Department of Urology, Affiliated Hospital of North Sichuan Medical College, Nanchong, Sichuan, China.
Department of Urology, The First Affiliated Hospital of Jinan University, Guangzhou, China.
Genes Genomics. 2021 Jul;43(7):807-814. doi: 10.1007/s13258-021-01093-0. Epub 2021 Apr 23.
PTX is widely used in cancer treatments.
In this paper, we explored the role and potential molecular mechanism of propofol in regulating PTX sensitivity in PC cells.
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.
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.
Propofol enhanced paclitaxel sensitivity in prostatic cancer cells through modulation of HOTAIR in vitro.
PTX 被广泛应用于癌症治疗。
本文旨在探讨丙泊酚在调节 PC 细胞对 PTX 敏感性中的作用及其潜在分子机制。
采用不同浓度的 PTX（10 nM、50 nM）、丙泊酚（150 μM、300 μM）或转染过表达 HOTAIR 质粒处理前列腺癌细胞系 PC3。采用 RT-qPCR 分析 HOTAIR 的表达。采用流式细胞术观察 PC3 细胞凋亡情况，CCK-8 法评估细胞活力。此外，采用 Western blot 法检测凋亡相关基因 Bcl-2 和 Bax。采用 ELISA 法监测 E-钙黏蛋白、N-钙黏蛋白和波形蛋白的蛋白浓度。
PTX 呈剂量依赖性显著增加 PC3 细胞凋亡，降低细胞活力。此外，Bcl-2 蛋白表达明显受到抑制，而 Bax 蛋白表达水平升高。进一步研究发现，随着 PTX 处理的增加，E-钙黏蛋白蛋白浓度增加，而 N-钙黏蛋白和波形蛋白减少。PTX 处理后 HOTAIR 表达下降，而过表达 HOTAIR 可诱导细胞活力、上皮间质转化（EMT）并抑制细胞凋亡。丙泊酚增强了 PTX 的作用，而过表达 HOTAIR 则部分逆转了这一作用。
丙泊酚通过调节 HOTAIR 增强了前列腺癌细胞对紫杉醇的敏感性。
