| 胡慧玲,李惠武,朱世茂,等.食管癌细胞中脂多糖对肿瘤坏死因子 α诱导程序性细胞死亡配体 1表达的影响[J].安徽医药,2023,27(8):1568-1572. |
| 食管癌细胞中脂多糖对肿瘤坏死因子 α诱导程序性细胞死亡配体 1表达的影响 |
| Effects of LPS on TNF-α induced PD-L1 expression in esophageal cancer cells |
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| DOI：10.3969/j.issn.1009-6469.2023.08.017 |
| 中文关键词: 食管肿瘤 癌，鳞状细胞 肿瘤坏死因子 α 脂多糖 Jak2/Stat3信号通路 程序性细胞死亡配体 1 |
| 英文关键词: Esophageal neoplasms Carcinoma, squamous cell Tumor necrosis factor-alpha Lipopolysaccharides Jak2/ Stat3 signaling pathway Programmed cell death ligand1 |
| 基金项目:国家自然科学基金资助项目( 81660459) |
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| 中文摘要: |
| 目的探讨在食管鳞癌 Eca-109细胞中脂多糖(LPS)通过 Jak2/Stat3信号通路对肿瘤坏死因子 α(TNF-α)诱导程序性细胞死亡配体 1(PD-L1)表达的影响及意义。方法 2020年 5―10月，在 TNF-α诱导下，分别使用 LPS干预食管鳞癌 Eca-109细胞 3、6、12、24 h以及不同浓度的 LPS干预食管鳞癌 Eca-109细胞 24 h，应用蛋白质印迹法检测 p-Jak2、p-Stat3、PD-L1蛋白表达水平的变化；应用流式细胞技术检测 LPS干预对 Eca-109细胞凋亡的影响。结果与对照组相比， TNF-α组中 p-Jak2蛋白表达(0.79±0.05比 0.63±0.11)、 p-Stat3蛋白表达( 1.48±0.24比 0.45±0.08)、 PD-L1蛋白表达( 0.92±0.15比 0.55±0.11)均升高( P<0.05)，同时 LPS组中凋亡率［(8.20±1.65)%比( 4.77±0.15)%］和 TNF-α+LPS干预组中凋亡率［(7.63±1.37)%比( 4.77±0.15)%］明显升高(P<0.05)。与 TNF-α组相比， TNF-α+LPS干预组中 p-Jak2蛋白表达( 0.46±0.05比 0.79±0.05)、 p-Stat3蛋白表达( 1.10±0.22比1.48±0.24)、 PD-L1蛋白表达( 0.59±0.08比 0.92±0.15)明显降低( P<0.05)。 LPS的干预下调 p-Jak2、p-Stat3、PD-L1的蛋白表达且呈浓度依赖性。结论 LPS通过干预 Jak2/Stat3信号通路下调 PD-L1的表达水平从而对食管鳞癌 Eca-109细胞的免疫逃逸机制进行调控，为进一步探索 LPS干预食管癌发生发展的分子机制提供了实验基础。 |
| 英文摘要: |
| Objective To investigate the effect of LPS on TNF-α induced PD-L1 expression in esophageal squamous cell carcinoma Eca-109 cells through Jak2/Stat3 signaling pathway.Methods From May to October 2020,Eca-109 cells of esophageal squamous cellcarcinoma were treated with LPS for 3,6,12,24 hours and different concentrations of LPS for 24 hours under TNF-α induction. The pro tein levels of p-Jak2, p-Stat3 and PD-L1 were detected by Western blotting. Flow cytometry was used to detect the effect of LPS on apoptosis of ECA-109 cells.Results Compared with the control group, p-jak2 (0.79±0.05 vs. 0.63±0.11),p-STAT3 (1.48±0.24 vs. 0.45± 0.08),and PD-L1 protein expression (0.92±0.15 vs. 0.55±0.11) in the TNF-α group were increased (P<0.05).Meanwhile, the apoptosis rate of LPS group [(8.20±1.65)% vs. (4.77±0.15)% ] and TNF-α +LPS group [(7.63±1.37)% vs. (4.77±0.15)% ] were significantly in creased (P<0.05).Compared with TNF-α group, p-JAK2 protein expression in TNF-α+LPS intervention group (0.46±0.05 vs. 0.79±0.05), p-STAT3 protein expression (1.10±0.22 vs. 1.48±0.24) and PD-L1 protein expression (0.59±0.08 vs. 0.92±0.15) were significantly de creased (P<0.05).LPS intervention down-regulated the protein expression of p-JAK2,p-STAT3 and PD-L1 in a concentration-dependent manner.Conclusion LPS regulates the immune escape mechanism of esophageal squamous cell carcinoma Eca-109 cells by down-regulating the expression level of PD-L1 through intervening in the Jak2/Stat3 signaling pathway, which provides an experimental basisfor further exploration of the molecular mechanism of LPS's intervention in the occurrence and development of esophageal carcinoma. |
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