SMC4 serves as a potential marker for the diagnosis and prognosis of colon adenocarcinoma.

IF 3.5 3区 医学
Dawei Yang, Wenxin Cheng, Ying Liu, Liang Ma, Yao Sun, Hongzhen Wang, Haifeng Liu, Li Nan, Yang Yang, Xinyue Wang
{"title":"SMC4 serves as a potential marker for the diagnosis and prognosis of colon adenocarcinoma.","authors":"Dawei Yang, Wenxin Cheng, Ying Liu, Liang Ma, Yao Sun, Hongzhen Wang, Haifeng Liu, Li Nan, Yang Yang, Xinyue Wang","doi":"10.1177/03946320241286565","DOIUrl":null,"url":null,"abstract":"<p><strong>Objective: </strong>We aimed to explore the role of structural maintenance of chromosomes 4 (SMC4) in malignant progression and immunology of colon adenocarcinoma (COAD).</p><p><strong>Methods: </strong>The expression, genetic and protein features, and immune cell infiltration of SMC4 in pan-cancer were provided by public databases and websites. The protein expression of SMC4 in COAD tissues was screened by immunohistochemical assay. Si-RNA-mediated transfection was performed in COAD cells and the proliferation viability was measured using MTT, colony formation and EdU assays. Cell autophagy was detected by AO staining, western blots, and immunofluorescence staining. The migratory ability was determined using scratch and transwell assays. The expression of epithelial-to-mesenchymal transition (EMT) markers and transcriptional factors were detected using western blots.</p><p><strong>Results: </strong>The expression of SMC4 was upregulated in pan-cancer and had relationships with prognosis, TMB, and MSI of cancer patients. Particularly, SMC4 protein was highly expressed in COAD tissues and correlated with poor prognosis of patients. Depletion of SMC4 inhibited cell proliferation, induced autophagy, and decreased migration through EMT progression in COAD cells. In addition, SMC4 was associated with infiltration of neutrophils, M2 macrophages, and CD4 + T cells in COAD, and had positive association with M2 macrophage markers and immune checkpoints.</p><p><strong>Conclusion: </strong>SMC4 was correlated with patients' poor prognosis, proliferation, metastasis, and immune cell infiltrates, and might function as a potential diagnosis and prognostic biomarker in COAD.</p>","PeriodicalId":48647,"journal":{"name":"International Journal of Immunopathology and Pharmacology","volume":"38 ","pages":"3946320241286565"},"PeriodicalIF":3.5000,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11490969/pdf/","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"International Journal of Immunopathology and Pharmacology","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1177/03946320241286565","RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 0

Abstract

Objective: We aimed to explore the role of structural maintenance of chromosomes 4 (SMC4) in malignant progression and immunology of colon adenocarcinoma (COAD).

Methods: The expression, genetic and protein features, and immune cell infiltration of SMC4 in pan-cancer were provided by public databases and websites. The protein expression of SMC4 in COAD tissues was screened by immunohistochemical assay. Si-RNA-mediated transfection was performed in COAD cells and the proliferation viability was measured using MTT, colony formation and EdU assays. Cell autophagy was detected by AO staining, western blots, and immunofluorescence staining. The migratory ability was determined using scratch and transwell assays. The expression of epithelial-to-mesenchymal transition (EMT) markers and transcriptional factors were detected using western blots.

Results: The expression of SMC4 was upregulated in pan-cancer and had relationships with prognosis, TMB, and MSI of cancer patients. Particularly, SMC4 protein was highly expressed in COAD tissues and correlated with poor prognosis of patients. Depletion of SMC4 inhibited cell proliferation, induced autophagy, and decreased migration through EMT progression in COAD cells. In addition, SMC4 was associated with infiltration of neutrophils, M2 macrophages, and CD4 + T cells in COAD, and had positive association with M2 macrophage markers and immune checkpoints.

Conclusion: SMC4 was correlated with patients' poor prognosis, proliferation, metastasis, and immune cell infiltrates, and might function as a potential diagnosis and prognostic biomarker in COAD.

SMC4 是诊断和预后结肠腺癌的潜在标志物。
目的我们旨在探讨 4 号染色体结构维护(SMC4)在结肠腺癌(COAD)恶性进展和免疫学中的作用:方法:SMC4在泛癌症中的表达、遗传和蛋白特征以及免疫细胞浸润均由公共数据库和网站提供。免疫组化法检测 COAD 组织中 SMC4 蛋白的表达。在 COAD 细胞中进行 Si-RNA 介导的转染,并使用 MTT、菌落形成和 EdU 检测法测定细胞的增殖活力。通过 AO 染色、Western 印迹和免疫荧光染色检测细胞自噬。细胞迁移能力通过划痕法和转孔法检测。通过 Western 印迹检测上皮细胞向间质转化(EMT)标志物和转录因子的表达:结果:SMC4在泛癌症中表达上调,并与癌症患者的预后、TMB和MSI有关。特别是,SMC4 蛋白在 COAD 组织中高表达,并与患者的不良预后相关。消耗 SMC4 可抑制 COAD 细胞增殖,诱导自噬,并通过 EMT 进展减少迁移。此外,SMC4 与 COAD 中的中性粒细胞、M2 巨噬细胞和 CD4 + T 细胞的浸润有关,并与 M2 巨噬细胞标记和免疫检查点呈正相关:结论:SMC4与患者的不良预后、增殖、转移和免疫细胞浸润相关,可作为COAD潜在的诊断和预后生物标志物。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
求助全文
约1分钟内获得全文 求助全文
来源期刊
International Journal of Immunopathology and Pharmacology
International Journal of Immunopathology and Pharmacology Immunology and Microbiology-Immunology
自引率
0.00%
发文量
88
期刊介绍: International Journal of Immunopathology and Pharmacology is an Open Access peer-reviewed journal publishing original papers describing research in the fields of immunology, pathology and pharmacology. The intention is that the journal should reflect both the experimental and clinical aspects of immunology as well as advances in the understanding of the pathology and pharmacology of the immune system.
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
确定
请完成安全验证×
copy
已复制链接
快去分享给好友吧!
我知道了
右上角分享
点击右上角分享
0
联系我们:info@booksci.cn Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。 Copyright © 2023 布克学术 All rights reserved.
京ICP备2023020795号-1
ghs 京公网安备 11010802042870号
Book学术文献互助
Book学术文献互助群
群 号:481959085
Book学术官方微信