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合并感染……的肝细胞癌患者的血清蛋白质组学和代谢组学分析

Serum proteomic and metabolomic profiling of hepatocellular carcinoma patients co-infected with .

作者信息

Tang Zeli, Wei Caibiao, Deng Xueling, Lin Qiumei, Hu Qiping, Li Shitao, Wang Jilong, Wu Yuhong, Liu Dengyu, Fang Min, Zhan Tingzheng

机构信息

Department of Cell Biology and Genetics, School of Basic Medical Sciences, Guangxi Medical University, Nanning, China.

Key Laboratory of Longevity and Aging-related Diseases of Chinese Ministry of Education, Guangxi Medical University, Nanning, China.

出版信息

Front Immunol. 2025 Jan 7;15:1489077. doi: 10.3389/fimmu.2024.1489077. eCollection 2024.

DOI:10.3389/fimmu.2024.1489077
PMID:39840062
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11746118/
Abstract

BACKGROUND

() infection is a significant risk factor for hepatocellular carcinoma (HCC), yet its underlying mechanisms remain poorly understood. This study aimed to investigate the impact of infection on the serum proteomic and metabolomic profiling of HCC patients, focusing on the potential mechanisms.

METHOD

A retrospective clinical analysis was conducted on 1121 HCC patients, comparing those with and without infection. The influence of on serum proteome and metabolome in HCC was further assessed.

RESULT

infection correlated with a younger age at cancer onset, male predominance, advanced cancer stage, liver cirrhosis, and microvascular invasion in HCC patients. It also associated with shorter overall survival (OS) and recurrence-free survival (RFS). The levels of blood lipids (e.g., APO-A, HDL-C, and TG) were significantly altered after infection. Proteomic and metabolomic analyses revealed metabolic reprogramming caused by , with excessive depletion of argininosuccinate synthase (ASS) and D-glucose as potential factors in -associated HCC malignancy. Key molecules ILF2, CNN2, OLFM4, NOTCH3, and LysoPA were implicated in HCC progression. Furthermore, triggered inflammation, insulin resistance, and pro-tumor immune escape, and exacerbated the complication of degenerative diseases.

CONCLUSION

This study not only provides compelling evidence for elucidating the mechanisms underlying -mediated HCC development but also identifies potential therapeutic targets for HCC patients co-infected with .

摘要

背景

()感染是肝细胞癌(HCC)的一个重要危险因素,但其潜在机制仍知之甚少。本研究旨在探讨()感染对HCC患者血清蛋白质组和代谢组谱的影响,重点关注潜在机制。

方法

对1121例HCC患者进行回顾性临床分析,比较有无()感染的患者。进一步评估()对HCC患者血清蛋白质组和代谢组的影响。

结果

()感染与HCC患者癌症发病年龄较轻、男性占主导、癌症晚期、肝硬化和微血管侵犯相关。它还与较短的总生存期(OS)和无复发生存期(RFS)相关。()感染后血脂水平(如载脂蛋白A、高密度脂蛋白胆固醇和甘油三酯)显著改变。蛋白质组学和代谢组学分析揭示了()导致的代谢重编程,精氨琥珀酸合酶(ASS)和D-葡萄糖的过度消耗是()相关HCC恶性肿瘤的潜在因素。关键分子白细胞介素增强子结合因子2(ILF2)、腱膜蛋白Cnn2(CNN2)、乳脂肪球表皮生长因子8(OLFM4)、Notch信号通路受体3(NOTCH3)和溶血磷脂酸(LysoPA)与HCC进展有关。此外,()引发炎症、胰岛素抵抗和促肿瘤免疫逃逸,并加重退行性疾病的并发症。

结论

本研究不仅为阐明()介导的HCC发展机制提供了有力证据,还为合并()感染的HCC患者确定了潜在的治疗靶点。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e35d/11746118/b1a291af45d4/fimmu-15-1489077-g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e35d/11746118/68536492083f/fimmu-15-1489077-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e35d/11746118/3b5b0dcfce39/fimmu-15-1489077-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e35d/11746118/9498f51cbc3c/fimmu-15-1489077-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e35d/11746118/a5ee8aa510e2/fimmu-15-1489077-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e35d/11746118/cb44501360f4/fimmu-15-1489077-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e35d/11746118/b5aedc77e51e/fimmu-15-1489077-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e35d/11746118/d4cb13a5f869/fimmu-15-1489077-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e35d/11746118/7d4d483a98e6/fimmu-15-1489077-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e35d/11746118/b1a291af45d4/fimmu-15-1489077-g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e35d/11746118/68536492083f/fimmu-15-1489077-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e35d/11746118/3b5b0dcfce39/fimmu-15-1489077-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e35d/11746118/9498f51cbc3c/fimmu-15-1489077-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e35d/11746118/a5ee8aa510e2/fimmu-15-1489077-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e35d/11746118/cb44501360f4/fimmu-15-1489077-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e35d/11746118/b5aedc77e51e/fimmu-15-1489077-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e35d/11746118/d4cb13a5f869/fimmu-15-1489077-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e35d/11746118/7d4d483a98e6/fimmu-15-1489077-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e35d/11746118/b1a291af45d4/fimmu-15-1489077-g009.jpg

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