[1]刘立威,林俊豪,陈逢生.ARHGAP10基因在肺腺癌中的表达及其机制[J].中国医学物理学杂志,2023,40(5):653-660.[doi:1005-202X(2023)05-0653-08]
 LIU Liwei,LIN Junhao,CHEN Fengsheng.Expression of ARHGAP10 in lung adenocarcinoma and relevant mechanisms[J].Chinese Journal of Medical Physics,2023,40(5):653-660.[doi:1005-202X(2023)05-0653-08]
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ARHGAP10基因在肺腺癌中的表达及其机制()
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《中国医学物理学杂志》[ISSN:1005-202X/CN:44-1351/R]

卷:
40卷
期数:
2023年第5期
页码:
653-660
栏目:
其他(激光医学等)
出版日期:
2023-05-26

文章信息/Info

Title:
Expression of ARHGAP10 in lung adenocarcinoma and relevant mechanisms
文章编号:
R318;R734.2
作者:
刘立威12林俊豪1陈逢生1
1.南方医科大学中西医结合医院肿瘤中心, 广东 广州 510315; 2.南方医科大学附属何贤纪念医院(广州市番禺区何贤纪念医院), 广东 广州 511400
Author(s):
LIU Liwei12 LIN Junhao1 CHEN Fengsheng1
1. Cancer Center, Hospital of Integrated TCM and Western Medicine, Southern Medical University, Guangzhou 510315, China 2. Affiliated Hexian Memorial Hospital, Southern Medical University (Hexian Memorial Hospital of Panyu District), Guangzhou 511400, China
关键词:
Rho GTPase活化蛋白10肺腺癌免疫治疗生物信息学分析
Keywords:
Keywords: Rho GTPase activating protein 10 lung adenocarcinoma immunotherapy bioinformatics analysis
DOI:
1005-202X(2023)05-0653-08
文献标志码:
A
摘要:
目的:基于生物信息学技术探讨Rho GTPase活化蛋白10(ARHGAP10)在肺腺癌发生发展中的潜在分子机制,为后续深入研究提供生物信息学证据。方法:通过利用TCGA数据库,获取肺腺癌患者RNA高通量序列及相关患者的临床资料,其中包括514例肺腺癌患者的癌组织以及59例相关的癌旁组织;GSE115002肺腺癌基因芯片数据从GEO下载,芯片包含52例肺腺癌患者的癌组织和匹配的癌旁正常组织。通过R语言技术比较ARHGAP10在TCGA和GSE115002中肺腺癌组织和癌旁正常组织之间表达差异,并进一步分析ARHGAP10表达与肺癌患者临床预后的相关性;挖掘两个数据库中ARHGAP10重叠基因,对重叠基因进行GO和KEGG富集分析,采用STRING数据库获取ARHGAP10的相关基因互作蛋白网络,TIMER数据库分析ARHGAP10与免疫浸润的相关性。结果:与癌旁正常组织相比较,肺腺癌组织中ARHGAP10呈现低表达状态(P<0.01)。与ARHGAP10低表达组相比较,ARHGAP10高表达患者拥有更长的总生存期和无进展生存期(P<0.05)。TCGA和GSE115002肺腺癌数据库中ARHGAP10的共同相关基因共133个,与MAPK、PI3K-AKT等信号通路以及细胞外基质受体结合、肌动蛋白细胞骨架、肿瘤信号通路等生物学进程相关。本研究发现PRELP、LIMS2、PPAP2B、MRPL42、SRP9、TSNAX等蛋白在ARHGAP10相互作用网络中发挥重要作用,ARHGAP10与DC细胞、中性粒细胞浸润正相关,与PD-L1表达呈正相关。结论:ARHGAP10在肺腺癌中起抑癌作用,与肺腺癌的生存预后正相关,可作为肺腺癌患者潜在的临床预后标志物。
Abstract:
Abstract: Objective To investigate the role and potential molecular mechanisms of Rho GTPase activating protein 10 (ARHGAP10) in the occurrence and development of lung adenocarcinoma using bioinformatics analysis, thereby providing a bioinformatics basis for further study. Methods The high-throughput RNA sequences of lung adenocarcinoma patients and relative clinical data were obtained from TCGA database which included cancer tissue from 514 lung adenocarcinoma patients and adjacent normal tissues from 59 patients. GSE115002 lung adenocarcinoma gene chip data was downloaded from GEO, and the chip contained the cancer tissue and adjacent normal tissues from 52 lung adenocarcinoma patients and the matched normal adjacent tissues. The differences in the expression of ARHGAP10 between lung adenocarcinoma tissues and adjacent normal tissues in TCGA and GSE115002 were analyzed using R language, and the correlation between ARHGAP10 expression and clinical prognosis of lung cancer patients was further explored. GO and KEGG pathway enrichment analyses were carried out on the overlapping genes in the two databases. The STRING database was used to construct the interaction protein network of ARHGAP10-related genes (ARGs), and the correlation between ARHGAP10 and immune infiltration was analyzed using TIMER database. Results ARHGAP10 had lower expression in lung adenocarcinoma tissues than in adjacent normal tissues (P<0.01), and lung adenocarcinoma patients with high ARHGAP10 expression had longer overall survival and progression-free survival (P<0.05). There were 133 ARGs in the TCGA and GSE115002 databases, involving MAPK, PI3K-AKT signaling pathway, extracellular matrix receptor binding, actin cytoskeleton, tumor signaling pathway and other biological processes. PRELP, LIMS2, PPAP2B, MRPL42, SRP9 and TSNAX were found to play key roles in the protein interaction network of ARGs. ARHGAP10 was positively correlated with DC cells and neutrophil infiltration, as well as PD-L1 expression. Conclusion ARHGAP10 which has an inhibitory effect on lung adenocarcinoma and is positively correlated with the survival and clinical prognosis of lung adenocarcinoma can serve as a potential prognostic marker for lung adenocarcinoma.

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备注/Memo

备注/Memo:
【收稿日期】2023-01-11 【基金项目】国家自然科学基金(81872251);广东省自然科学基金(2020A1515010093, 2021A1515012104);南方医科大学中西医结合医院院长基金(1202102002) 【作者简介】刘立威,硕士,主治医师,研究方向:肺肿瘤发生发展机制,E-mail: gzpyllw@163.com 【通信作者】陈逢生,副主任医师,硕士生导师,研究方向:肝、肺恶性肿瘤发生机制,E-mail: fsc0126@163.com
更新日期/Last Update: 2023-05-26