[肝细胞癌中GIT1、M2巨噬细胞浸润高表达与预后的相关性研究]。

Q3 Medicine
B B Su, C Zhang, B S Wei, J Cao, R Peng, D Y Tu, G Q Jiang, S J Jin, D S Bai
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引用次数: 0

摘要

目的:探讨G蛋白偶联受体激酶相互作用蛋白1 (GIT1)在肝细胞癌(HCC)肿瘤微环境中的表达、预后及作用。方法:选取2015年1月至2021年12月在江苏省扬州大学附属苏北人民医院行肝细胞癌手术全切除术的140例患者的临床资料。采集肿瘤组织及邻近组织标本进行免疫组化分析。根据GIT1表达情况将患者分为高表达组和低表达组。采用Cox回归分析影响HCC患者预后的危险因素。将15对癌组织与癌旁组织随机配对,进行定量聚合酶链反应(RT-PCR)、免疫印迹(WB)和免疫组化分析。构建人肝癌细胞系HepG2、HuH7、MHCC97-H和小鼠肝癌细胞系Hepa 1-6的GITI敲除或过表达细胞系。流式细胞术分析其对M2巨噬细胞极化的影响。建立小鼠肿瘤模型。绘制过表达GIT1的肿瘤组织生长曲线。采用肿瘤学、Kaplan-Meier Plotter、UALCAN、GEPIA等数据库对肿瘤基因组图谱(Cancer Genome Atlas, TCGA)数据进行生物信息学分析,探讨GIT1在HCC患者中的差异表达及其对预后的影响。结果:生物信息学分析显示,GIT1在HCC组织中的表达水平明显高于正常肝组织(PHR=2.562, 95%CI: 0.231 ~ 0.704, Pr=0.545, ppppp)。结论:GIT1在HCC中具有预后生物标志物作用,通过其高表达促进肿瘤进展,增强M2巨噬细胞浸润。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
[Study on the correlation between high expression of GIT1 and M2 macrophage infiltration and prognosis in hepatocellular carcinoma].

Objective: To investigate the expression, prognosis, and role of G protein-coupled receptor kinase-interacting protein 1 (GIT1) in patients with hepatocellular carcinoma (HCC) tumor micro environments. Methods: Clinical data of 140 cases who underwent complete HCC surgical resection from January 2015 to December 2021 in Subei People's Hospital affiliated to Yangzhou University, Jiangsu Province, were included. Tumor tissue and adjacent tissue samples were collected for immunohistochemical analysis. The patients were divided into a high expression group and a low expression group according to the expression of GIT1. Cox regression was used to analyze the risk factors for prognosis in patients with HCC. Fifteen pairs of cancer tissues and adjacent tissues were randomly matched for quantitative polymerase chain reaction (RT-PCR), western blot (WB), and immunohistochemical analysis. GITI knockout or overexpression cell lines of human hepatoma cell lines HepG2, HuH7 and MHCC97-H, and mouse hepatoma cell line Hepa 1-6 were constructed. The effects on M2 macrophage polarization were analyzed by flow cytometry. A mice tumor model was constructed. The growth curve of tumor tissue overexpressing GIT1 was plotted. Bioinformatics analysis of the Cancer Genome Atlas (TCGA) data was performed using OncoLnc, Kaplan-Meier Plotter, UALCAN, and GEPIA databases to explore the differential expression of GIT1 in HCC patients and its effect on prognosis. Results: Bioinformatics analysis showed that the expression level of GIT1 was significantly higher in HCC tissues than in normal liver tissues (P<0.05). RT-PCR and WB experiments showed that GIT1 was highly expressed in HCC. The follow-up results showed that high expression of GIT1 was associated with poor prognosis in patients with HCC. The high expression of GIT1 was an independent risk factor for the prognosis in patients with HCC (HR=2.562, 95%CI: 0.231-0.704, P<0.05). Functional enrichment analysis combined with TIMER database analysis found that GIT1 expression level was associated with multiple immune cell infiltrations in HCC, but the correlation coefficient with macrophage infiltration was the highest (r=0.545, P<0.001). Mice tumorigenesis experiments showed that the tumor volume of GIT1-overexpressing mice was significantly increased (P<0.05). Additionally, flow cytometry indicated that after GIT1 overexpression, there was a low degree of M1 infiltration/polarization (wild type: 5.06%±0.11%, overexpression type: 4.09%±0.04%; P<0.05) and a high degree of M2 infiltration/polarization (wild type: 10.20%±0.33%, overexpression type: 14.7%±0.12%; P<0.05). Conclusion: GIT1 serves as a prognostic biomarker in HCC, promoting tumor progression through its high expression and enhances M2 macrophage infiltration.

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中华肝脏病杂志
中华肝脏病杂志 Medicine-Medicine (all)
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1.20
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7574
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