CTSG may inhibit disease progression in HIV-related lung cancer patients by affecting immunosuppression.

IF 3.1 2区医学 Q3 IMMUNOLOGY Infectious Agents and Cancer Pub Date : 2024-07-30 DOI:10.1186/s13027-024-00599-y

Xuan Yan, Shuoyan Wei, Yuexiang Yang, Zhangyan Zhao, Qingguo Wu, Haicheng Tang

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Abstract

Objectives: Lung cancer is an independent risk factor for pulmonary complications following HIV infection. This study aimed to examine the expression and clinical significance of Cathepsin G (CTSG) protein in both non-HIV and HIV-related lung cancers.

Methods: The data related to lung adenocarcinoma (LUAD) and lung squamous carcinoma (LUSC) in the TCGA dataset and the data related to healthy individuals in the GTEx dataset, the GEPIA2 database was used to excavate the distinction in the expression of CTSG protein in non-small cell lung cancer (NSCLC) tissues versus normal non-cancerous tissues. The Ualcan database was used to compare the differences in CTSG expression at different stages of LUAD and LUSC. Immunohistochemistry (IHC) was used to detect the expression of CTSG proteins in the pathological tissues of patients with HIV-related lung cancer and patients with lung cancer without co-infection, the Kaplan-Meier method was used for survival analysis.

Results: We observed that CTSG expression in NSCLC is lower compared to adjacent non-tumor tissues and correlates with NSCLC clinical stage. CTSG protein expression in HIV-related lung cancer tissues was lower than in adjacent tissues and lower than in lung cancer tissues without HIV infection, with a statistically significant difference (P < 0.05). It correlated with CD4 + T cell count and CD4+/CD8 + T cell ratio, as well as with the pathological type, distant metastasis, and clinical stage of HIV-related lung cancer, all with statistical significance (P < 0.05).

Conclusions: CTSG could potentially mitigate disease advancement in HIV-related lung cancer patients by inhibiting immune depletion, serving as a prospective immunotherapeutic target for both non-HIV and HIV-associated lung cancers.

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CTSG 可通过影响免疫抑制来抑制 HIV 相关肺癌患者的病情发展。

目的：肺癌是艾滋病病毒感染后肺部并发症的独立危险因素。本研究旨在探讨Cathepsin G（CTSG）蛋白在非HIV和HIV相关肺癌中的表达及其临床意义：方法：利用 TCGA 数据集中与肺腺癌（LUAD）和肺鳞癌（LUSC）相关的数据，以及 GTEx 数据集中与健康人相关的数据、GEPIA2 数据库，挖掘 CTSG 蛋白在非小细胞肺癌（NSCLC）组织与正常非癌组织中的表达差异。Ualcan数据库用于比较CTSG在LUAD和LUSC不同阶段的表达差异。免疫组化法（IHC）用于检测HIV相关肺癌患者和未合并感染的肺癌患者病理组织中CTSG蛋白的表达，Kaplan-Meier法用于生存分析：我们观察到，CTSG在NSCLC中的表达量低于相邻的非肿瘤组织，并且与NSCLC的临床分期相关。CTSG蛋白在HIV相关肺癌组织中的表达量低于邻近组织，也低于未感染HIV的肺癌组织，差异有统计学意义（P 结论：CTSG可能缓解NSCLC的临床分期：CTSG可抑制免疫耗竭，从而缓解HIV相关肺癌患者的病情发展，有望成为非HIV和HIV相关肺癌的免疫治疗靶点。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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来源期刊

Infectious Agents and Cancer ONCOLOGY-IMMUNOLOGY

CiteScore

5.80

自引率

2.70%

发文量

期刊介绍： Infectious Agents and Cancer is an open access, peer-reviewed online journal that encompasses all aspects of basic, clinical, epidemiological and translational research providing an insight into the association between chronic infections and cancer. The journal welcomes submissions in the pathogen-related cancer areas and other related topics, in particular: • HPV and anogenital cancers, as well as head and neck cancers; • EBV and Burkitt lymphoma; • HCV/HBV and hepatocellular carcinoma as well as lymphoproliferative diseases; • HHV8 and Kaposi sarcoma; • HTLV and leukemia; • Cancers in Low- and Middle-income countries. The link between infection and cancer has become well established over the past 50 years, and infection-associated cancer contribute up to 16% of cancers in developed countries and 33% in less developed countries. Preventive vaccines have been developed for only two cancer-causing viruses, highlighting both the opportunity to prevent infection-associated cancers by vaccination and the gaps that remain before vaccines can be developed for other cancer-causing agents. These gaps are due to incomplete understanding of the basic biology, natural history, epidemiology of many of the pathogens that cause cancer, the mechanisms they exploit to cause cancer, and how to interrupt progression to cancer in human populations. Early diagnosis or identification of lesions at high risk of progression represent the current most critical research area of the field supported by recent advances in genomics and proteomics technologies.