Feng Haipeng, Lin Bo, Zheng Yifei, Xu Junnv, Zhou Ying, Liu Kun, Zhu Mingyue, Li Mengsen
Hainan Provincial Key Laboratory of Carcinogenesis and Intervention, Hainan Medical College, Haikou, Hainan Province, China.
Department of Tumor Internal Medicine, Second affiliated Hospital of Hainan Medical College, Haikou, Hainan Province, China.
Cell J. 2020 Jul;22(Suppl 1):89-100. doi: 10.22074/cellj.2020.6894. Epub 2020 Jul 18.
Explore the effect of expression on Paclitaxel inhibiting growth of hepatocellular carcinoma (HCC) cells.
In the experimental study, HCC cell lines (HLE, Bel7402 and PLC/PRF/5) were treated with different concentrations of Paclitaxel (5-20 mg/ml) for 24 hours. HLE cells were transfected with -siRNA vector, while Bel7402 and PLC/PRF/5 cells were transfected with overexpressed GATA5 vector for 24 hours, followed by treatment of the cells with Paclitaxel (10 mg/ml) for 24 hours and subsequently 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2-H-tetrazolium bromide (MTT) assay to detect growth of HCC cells. Soft agar cultured was used to analyze formation of colony. Apoptosis of HCC cells were detected by Flow cytometer. Migration of HCC cells was observed by trawell assays. Western blotting and laser confocal microscopy were utilized to detect expression and location of the proteins.
Inhibiting expression of reduced sensitivity of HLE cells to Paclitaxel, while overexpression of increased sensitivity of Bel7402 cells and PLC/PRF/5 cells to Paclitaxel. Overexpression of played a role in stimulating Paclitaxel to inhibit growth, colony formation and migration, as well as enhance apoptosis in HCC cells. Overexpression of also promoted Paclitaxel to inhibit expression of reprogramming genes, such as Nanog, and in Bel7402 and PLC/PRF/5 cells. Inhibited expression of led to enhancement of the expression of CD44 and CD133, in HLE cells. Overexpression of was not only alone but also synergized with Paclitaxel to inhibit expression of CD44 and CD133 in Bel7402 or PLC/PRF/5 cells.
Overexpression of played a role in enhancing Paclitaxel to inhibit the malignant behaviors of HCC cells. It was involved in suppressing expression of the reprogramming genes and stemness markers. Targeting is an available strategy for applying paclitaxel to therapy of patients with HCC.
探讨[具体基因名称]表达对紫杉醇抑制肝癌（HCC）细胞生长的影响。
在实验研究中，将肝癌细胞系（HLE、Bel7402和PLC/PRF/5）用不同浓度的紫杉醇（5 - 20 mg/ml）处理24小时。HLE细胞用[具体基因名称]-siRNA载体转染，而Bel7402和PLC/PRF/5细胞用过表达GATA5载体转染24小时，随后用紫杉醇（10 mg/ml）处理细胞24小时，接着进行3-(4,5-二甲基-2-噻唑基)-2,5-二苯基-2-H-四氮唑溴盐（MTT）法检测肝癌细胞的生长。采用软琼脂培养分析集落形成。通过流式细胞仪检测肝癌细胞的凋亡。通过Transwell实验观察肝癌细胞的迁移。利用蛋白质印迹法和激光共聚焦显微镜检测蛋白质的表达和定位。
抑制[具体基因名称]表达降低了HLE细胞对紫杉醇的敏感性，而过表达[具体基因名称]增加了Bel7402细胞和PLC/PRF/5细胞对紫杉醇的敏感性。过表达[具体基因名称]在刺激紫杉醇抑制生长、集落形成和迁移以及增强肝癌细胞凋亡方面发挥作用。过表达[具体基因名称]还促进紫杉醇抑制Bel7402和PLC/PRF/5细胞中重编程基因如Nanog、[其他重编程基因名称]和[另一重编程基因名称]的表达。抑制[具体基因名称]表达导致HLE细胞中CD44和CD133表达增强。过表达[具体基因名称]不仅单独而且与紫杉醇协同抑制Bel7402或PLC/PRF/5细胞中CD44和CD133的表达。
过表达[具体基因名称]在增强紫杉醇抑制肝癌细胞恶性行为方面发挥作用。它参与抑制重编程基因和干性标志物的表达。靶向[具体基因名称]是将紫杉醇应用于肝癌患者治疗的一种可行策略。
