安徽医科大学学报2026，Vol.61Issue(2)：232-238,7.DOI:10.19405/j.cnki.issn1000-1492.2026.02.007
B7-H3分子通过SIRT1/p53信号途径抑制非小细胞肺癌细胞凋亡
B7-H3 molecule inhibits apoptosis of non-small cell lung cancer cells via the SIRT1/p53 signaling pathway
摘要
Abstract
Objective To explore the role of the histone deacetylase Sirtuin-1(SIRT1)/p53 signaling pathway in promoting apoptosis of non-small cell lung cancer cells(NSCLC)induced by the co-stimulatory molecule B7 homo-log 3(B7-H3).Methods The GEPIA 2 platform was used for survival analysis of NSCLC patients based on B7-H3 gene expression levels.The Gene Enrichment Analysis(GSEA)method was used to analyze the enrichment characteristics of B7-H3 molecules in the gene set of cell apoptosis.In the non-small cell lung cancer A549 cell line,B7-H3 was knocked down,and the protein expression levels of SIRT1 and p53 were detected by Western blot.B7-H3 was overexpressed in A549 cells and the apoptosis rate was analyzed by flow cytometry after Annexin V/PI double staining.Overexpression of B7-H3 and knockdown of SIRT1 were performed in A549 cell line.The ex-pression levels of p53 and apoptosis-related proteins B-cell lymphoma/leukemia-2(Bcl-2)and Bcl-2-associated X protein(Bax)were detected respectively by Western blot.Cell apoptosis rate was analyzed by flow cytometry after Annexin V/PI double staining.Results The overall survival of the B7-H3 high-expression group was significantly lower than that of the low-expression group(P<0.01).B7-H3 was significantly enriched in the cell apoptosis sig-naling pathway and the p53 signaling pathway(P<0.05).Compared with the control group,the expression of SIRT1 was significantly downregulated,and p53 was significantly upregulated in the B7-H3 knockdown group(both P<0.001).Overexpression of B7-H3 significantly up-regulated SIRT1 protein expression(P<0.05),down-regulated p53 expression(P<0.01),and markedly increased the Bcl-2/Bax ratio of apoptosis-related proteins(P<0.001).The results of Annexin V/PI double staining showed that the apoptosis rate of A549 cells with overex-pressed B7-H3 decreased(the apoptosis rate of the control group was 26.72%±4.13%,while that of the B7-H3 overexpression group was 13.87%±0.82%;P<0.01).In B7-H3-overexpressing cell lines,SIRT1 knockdown sig-nificantly reversed apoptosis(P<0.05),up-regulated p53 protein expression(P<0.001),and markedly reduced the Bcl-2/Bax ratio(P<0.001).Conclusion B7-H3 molecule inhibits the apoptosis of non-small cell lung cancer cells via the SIRT1/p53 signaling pathway.关键词
非小细胞肺癌/细胞凋亡/协同信号分子/B7-H3/SIRT1/p53Key words
non-small cell lung cancer/cell apoptosis/co-signalling molecules/B7-H3/SIRT1/p53分类
医药卫生引用本文复制引用
郑霖,钟剑鑫,牛可,徐晴,凌惠娟,朱亚玉,陈兵,陈礼文..B7-H3分子通过SIRT1/p53信号途径抑制非小细胞肺癌细胞凋亡[J].安徽医科大学学报,2026,61(2):232-238,7.基金项目
国家自然科学基金项目(编号:82404970) （编号:82404970）
安徽省高校自然科学研究重点项目(编号:2023AH053170) （编号:2023AH053170）
安徽省临床医学研究转化项目(编号:202304295107020019) Fund programs National Natural Science Foundation of China(No.82404970) （编号:202304295107020019）
Natural Science Research Project of Anhui Educational Committee(No.2023AH053170) （No.2023AH053170）
Clinical Medical Research Translational Project of Anhui Province(No.202304295107020019) （No.202304295107020019）
