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[1]郦曼桐,欧阳雨晴,丰小帆,等.IL-10/IL-10RA调控非小细胞肺癌细胞增殖和机制的研究[J].天津医科大学学报,2025,31(03):196-202.[doi:10.20135/j.issn.1006-8147.2025.03.0196]
　LI Mantong,OUYANG Yuqing,FENG Xiaofan,et al.Study on the regulation and mechanism of IL-10/IL-10RA in cell proliferation of non-small cell lung cancer cells[J].Journal of Tianjin Medical University,2025,31(03):196-202.[doi:10.20135/j.issn.1006-8147.2025.03.0196]
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IL-10/IL-10RA调控非小细胞肺癌细胞增殖和机制的研究(PDF)

《天津医科大学学报》[ISSN:1006-8147/CN:12-1259/R]

卷:
31卷
期数:
2025年03期
页码:
196-202
栏目:
肿瘤疾病专题
出版日期:
2025-05-20

文章信息/Info

Title:
Study on the regulation and mechanism of IL-10/IL-10RA in cell proliferation of non-small cell lung cancer cells
文章编号:
1006-8147(2025)03-0196-07
作者:
郦曼桐1; 2; 欧阳雨晴1; 丰小帆1; 杜玮1; 邓为民1
（1.天津医科大学基础医学院免疫学系，国家教育部免疫微环境与疾病重点实验室，天津300070；2.天津市血液中心，天津300110）
Author(s):
LI Mantong1; 2; OUYANG Yuqing1; FENG Xiaofan1; DU Wei1; DENG Weimin1
（1.Department of Immunology，School of Basic Medical Sciences，Tianjin Medical University，Key Laboratory of Diseases and Microenvironment of Ministry of Education of China，Tianjin 300070，China；2.Tianjin Blood Center，Tianjin 300110，China）
关键词:
IL-10; IL-10RA; 非小细胞肺癌; 细胞增殖
Keywords:
IL-10; IL-10RA; non-small cell lung cancer; energy metabolism
分类号:
R737.31
DOI:
10.20135/j.issn.1006-8147.2025.03.0196
文献标志码:
A
摘要:
目的：探讨白细胞介素（IL）-10/IL-10受体（IL-10RA）对非小细胞肺癌（NSCLC）细胞增殖的作用及机制。方法：利用HPA数据库分析NSCLC组织和正常肺组织中IL-10表达情况。利用GEO数据分析IL-10/IL-10RA影响细胞增殖的相关的通路。构建IL-10RA稳定转染的NSCLC细胞系，通过CCK-8及流式Annexin V-FITC/PI双染凋亡检测IL-10/IL-10RA对NSCLC细胞增殖和凋亡的影响。通过Western印迹检测下游信号通路相关蛋白的水平，CCK-8和流式Annexin V-FITC/PI双染凋亡实验检测哺乳动物雷帕霉素靶蛋白（mTOR）抑制剂（雷帕霉素）对过表达IL-10RA的NSCLC细胞增殖和凋亡的影响。结果：与正常肺组织相比，NSCLC组织中IL-10蛋白表达水平明显升高。生物信息学分析提示，高表达IL-10RA的肺癌细胞系细胞增殖通路上调。与空载组相比，IL-10RA过表达的H1975细胞中IL-10RA的mRNA（t=21.42，P＜0.000 1）和蛋白（t=29.83，P＜0.000 1）显著增加。与空载组相比，IL-10RA过表达的H1975细胞增殖增加（t=4.445 6、8.494、11.73，均P＜0.01）、细胞凋亡减少（t=7.366，P＜0.01）。与空载组相比，IL-10RA过表达的H1975细胞p-mTOR/mTOR增加（t=16.52，P＜0.000 1）。使用雷帕霉素可以抑制IL-10RA对H1975细胞的细胞增殖（t=4.12、6.131、5.77，均P＜0.01）、细胞凋亡（t=3.836，P＜0.05）影响。结论：IL-10/IL-10RA通过mTOR信号通路促进NSCLC细胞增殖。
Abstract:
Objective：To investigate the effect and mechanism of interleukin-10 （IL-10） /IL-10 receptor （IL-10RA） on cell proliferation of non-small cell lung cancer （NSCLC）. Methods：The expression of IL-10 in NSCLC tissues and normal lung tissues was analyzed by HPA databases. GEO data were used to analyze the related pathways of IL-10/IL-10RA affecting cell proliferation. NSCLC cell line stably transfected with IL-10RA was constructed. The effect of IL-10/IL-10RA on proliferation and apoptosis of NSCLC cells was detected by CCK-8 and flow cytometry Annexin V-FITC/PI double staining apoptosis. The levels of downstream signaling pathway related proteins were detected by Western blotting，and the effects of mammalian mTOR inhibitor （rapamycin） on proliferation and apoptosis of NSCLC cells overexpressed with IL-10RA were detected by CCK-8 and flow cytometry Annexin V-FITC/PI double staining apoptosis assay. Results：Compared with normal lung tissues，IL-10 protein expression levels in NSCLC tissues were significantly increased. Bioinformatics indicated that the proliferation pathways of lung cancer cell lines with high expression of IL-10RA were up-regulated. Compared with empty group，IL-10RA mRNA （t=21.42，P＜0.000 1） and protein （t=29.83，P＜0.000 1） expression levels in H1975 cells with IL-10RA overexpression were increased. Compared with empty group，IL-10RA overexpressed H1975 cells increased the proliferation （t=4.445 6，8.494，11.73，all P＜0.01） and decreased apoptosis （t=7.366，P＜0.01）. Compared with empty group，p-mTOR/mTOR increased in H1975 cells with IL-10RA overexpression （t=16.52，P＜0.000 1），and Rapamycin could inhibit the effects of IL-10RA on cell proliferation （t=4.12，6.131，5.77，all P<0.01） and apoptosis （t=3.836，P<0.05） of H1975 cells. Conclusion：IL-10/IL-10RA promotes the proliferation of NSCLC cell through the mTOR signaling pathway.

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备注/Memo

备注/Memo:
基金项目: 国家自然科学基金（82273340，81872319）；京津冀基础研究合作专项（20JCZXJC00140）
作者简介: 郦曼桐（1992-），女，主管护师，硕士在读，研究方向：免疫学；
通信作者：邓为民，E-mail：dengweimin@tmu.edu.cn；杜玮，E-mail：dw1022@tmu.edu.cn。
更新日期/Last Update: 2025-06-01