Hou Xin-Fang, Xu Lin-Ping, Song Hai-Yan, Li Shuai, Wu Chen, Wang Ju-Feng
Xin-Fang Hou, Shuai Li, Chen Wu, Ju-Feng Wang, Department of Medical Oncology, Affiliated Cancer Hospital of Zhengzhou University, Henan Cancer Hospital, Zhengzhou 450008, Henan Province, China.
World J Gastroenterol. 2017 Mar 14;23(10):1796-1803. doi: 10.3748/wjg.v23.i10.1796.
To explore the anti-tumor effects of esophageal cancer-related gene 2 (ECRG2) in combination with cisplatin (DDP) in DDP-resistant esophageal cancer cells (EC9706/DDP).
A drug-resistant cell model was established, with EC9706/DDP cells being treated with ECRG2 and/or DDP. Cell viability was examined by MTT assay. The rate of cell apoptosis was determined by flow cytometry. The mRNA expression levels of proliferating cell nuclear antigen (PCNA), metallothionein (MT), and p53 were determined by RT-PCR and PCNA, while MT and p53 protein expression levels were determined by western blotting.
The anti-proliferative effect of ECRG2 in combination with DDP was superior when compared to ECRG2 or DDP alone. The inhibition rate for the combination reached its peak (51.33%) at 96 h. The early apoptotic rates of the control, ECRG2 alone, DDP alone, and ECRG2 plus DDP groups were 5.71% ± 0.27%, 12.68% ± 0.61%, 14.15% ± 0.87%, and 27.96% ± 0.36%, respectively. Although all treatment groups were significantly different from the control group ( < 0.05), the combination treatment of ECRG2 plus DDP performed significantly better when compared to either ECRG2 or DDP alone ( < 0.05). The combination of ECRG2 and DDP significantly upregulated p53 mRNA and protein levels and downregulated PCNA mRNA and protein levels compared to ECRG2 or DDP alone ( < 0.05). However, no changes were seen in the expression of MT mRNA or protein.
in combination with DDP can inhibit viability and induce apoptosis in esophageal cancer DDP-resistant cells, possibly upregulation of expression and downregulation of expression. These findings suggest that the combination of ECRG2 and DDP may be a promising strategy for the clinical treatment of esophageal cancers that are resistant to DDP.
探讨食管癌相关基因2（ECRG2）联合顺铂（DDP）对顺铂耐药食管癌细胞（EC9706/DDP）的抗肿瘤作用。
建立耐药细胞模型，用ECRG2和/或DDP处理EC9706/DDP细胞。采用MTT法检测细胞活力。通过流式细胞术测定细胞凋亡率。采用RT-PCR测定增殖细胞核抗原（PCNA）、金属硫蛋白（MT）和p53的mRNA表达水平，采用蛋白质印迹法测定PCNA、MT和p53蛋白表达水平。
与单独使用ECRG2或DDP相比，ECRG2联合DDP的抗增殖作用更强。联合用药在96 h时抑制率达到峰值（51.33%）。对照组、单独使用ECRG2组、单独使用DDP组和ECRG2加DDP组的早期凋亡率分别为5.71%±0.27%、12.68%±0.61%、14.15%±0.87%和27.96%±0.36%。虽然所有治疗组与对照组相比差异均有统计学意义（<0.05），但ECRG2加DDP联合治疗组与单独使用ECRG2或DDP组相比效果显著更好（<0.05）。与单独使用ECRG2或DDP相比，ECRG2和DDP联合使用显著上调p53 mRNA和蛋白水平，下调PCNA mRNA和蛋白水平（<0.05）。然而，MT mRNA或蛋白表达未见变化。
联合DDP可抑制食管癌顺铂耐药细胞的活力并诱导其凋亡，可能与上调 表达和下调 表达有关。这些发现表明，ECRG2和DDP联合使用可能是临床治疗对DDP耐药食管癌的一种有前景的策略。
