| miR-586靶向TLR7调控食管癌细胞CaES-17的凋亡和增殖 |
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| 引用本文： | 陈 龙,李世清,罗 晖,唐小波,兰 超.miR-586靶向TLR7调控食管癌细胞CaES-17的凋亡和增殖[J].现代肿瘤医学,2022,0(16):2874-2880. |
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| 作者姓名： | 陈 龙 李世清 罗 晖 唐小波 兰 超 |
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| 作者单位： | 1.南充市中心医院消化内科；2.胸外科，四川 南充 637000 |
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| 基金项目： | 四川省医学科研青年创新项目（编号:KY_Q16046） |
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| 摘 要： | 目的:探讨miRNA调控食管癌细胞CaES-17的凋亡和增殖的潜在机制。方法:纳入2019年06月至2020年06月在我院接受治疗的食管癌患者6例，采集其食管癌组织和癌旁组织后抽取总RNA进行miRNA高通量测序。在食管癌细胞CaES-17中过表达食管癌组织和癌旁组织中的差异miRNA，检测食管癌细胞CaES-17的凋亡和增殖情况。通过TargentScan7.2在线分析和荧光素酶报告实验分析miRNA的靶标mRNA。结果:6例患者的食管癌组织和癌旁组织通过高通量测序发现hsa-miR-30d-5p、hsa-miR-6818-5p、hsa-miR-525-5p、hsa-miR-1909-3p、hsa-miR-212-5p、hsa-miR-586、hsa-miR-1286、hsa-miR-365b-3p、hsa-miR-30e-5p、hsa-miR-4317在食管癌组织和癌旁组织中的表达差异在8倍以上，并且食管癌组织均高于癌旁组织。干扰上述miRNA后，发现干扰miR-586能够抑制食管癌细胞CaES-17的增殖水平和迁移水平，提高凋亡水平。过表达miR-586后，食管癌细胞CaES-17的凋亡水平下降，增殖水平和迁移水平上升。TargentScan7.2在线分析和荧光素酶报告实验发现miR-586靶向TLR7的3' 端非编码区。敲低TLR7后，食管癌细胞CaES-17的凋亡水平下降，增殖水平和迁移水平上升。过表达TLR7后，食管癌细胞CaES-17的凋亡水平上升，增殖水平和迁移水平下降。但是，同时干扰miR-586和敲低TLR7后，相比于对照食管癌细胞，食管癌细胞CaES-17的凋亡水平和增殖水平无显著差异。结论:miR-586通过靶向TLR7的3' 端非编码区，降解了TLR7的mRNA，抑制了TLR7的蛋白翻译，最终抑制了食管癌细胞CaES-17的凋亡、促进了食管癌细胞CaES-17的增殖。
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| 关 键 词： | miR-586 TLR7 食管癌 CaES-17 凋亡 增殖 |
miR-586 targeting TLR7 to regulate the apoptosis and proliferation of esophageal cancer cells CaES-17 |
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| CHEN Long,LI Shiqing,LUO Hui,TANG Xiaobo,LAN Chao.miR-586 targeting TLR7 to regulate the apoptosis and proliferation of esophageal cancer cells CaES-17[J].Journal of Modern Oncology,2022,0(16):2874-2880. |
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| Authors: | CHEN Long LI Shiqing LUO Hui TANG Xiaobo LAN Chao |
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| Affiliation: | 1.Department of Digestive Medicine;2.Department of Thoracic Surgery,Nanchong Central Hospital,Sichuan Nanchong 637000,China. |
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| Abstract: | Objective:To investigate the potential mechanism of apoptosis and proliferation of esophageal cancer cells CaES-17 regulated by miRNA.Methods:Six cases of esophageal cancer patients who received treatment from June 2019 to June 2020 in our hospital were enrolled.After collecting their esophageal cancer tissues and paracancerous tissues,total RNA was extracted for miRNA high-throughput sequencing.The differential miRNAs in esophageal cancer tissues and paracancerous tissues were overexpressed in esophageal cancer cells CaES-17,and the apoptosis and proliferation of esophageal cancer cells CaES-17 were detected.The target mRNA of miRNA was analysed through TargentScan7.2 online analysis and luciferase report experiment.Results:The expressions of hsa-miR-30d-5p,hsa-miR-6818-5p,hsa-miR-525-5p,hsa-miR-1909-3p,hsa-miR-212-5p,hsa-miR-586,hsa-miR-1286,hsa-miR-365b-3p,hsa-miR-30e-5p and hsa-miR-4317 in esophageal cancer tissues and paracancerous tissues were more than 8 times different,and their expressions in esophageal cancer tissues were all higher than the paracancerous tissues.After the above miRNA interference,it was found that interference of miR-586 could inhibit the proliferation and migration levels of esophageal cancer cells CaES-17,and improve the apoptosis level.After overexpression of miR-586,the apoptosis level of esophageal cancer cells CaES-17 decreased,and the proliferation and migration levels increased.TargentScan7.2 online analysis and luciferase reporting assay revealed that miR-586 targeted the 3'-terminal non-coding region of TLR7.After TLR7 knockdown,the apoptosis level of esophageal carcinoma cells CaES-17 decreased,and the proliferation and migration levels increased.After overexpression of TLR7,the apoptosis level of esophageal carcinoma cells CaES-17 increased,and the proliferation and migration levels decreased.However,there was no significant difference in apoptosis level and proliferation level of esophageal cancer cells CaES-17 after both miR-586 interference and TLR7 knockdown,compared with control.Conclusion:miR-586 degrades TLR7 mRNA and inhibits TLR7 protein translation by targeting the 3'-terminal non-coding region of TLR7,and ultimately inhibits the apoptosis of esophageal cancer cells CaES-17 and promotes the proliferation of esophageal cancer cells CaES-17. |
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| Keywords: | miR-586 TLR7 esophageal cancer CaES-17 apoptosis proliferation |
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