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胶原蛋白1A1作为卵巢癌临床特征和免疫微环境的新解码因子。

Col1A1 as a new decoder of clinical features and immune microenvironment in ovarian cancer.

作者信息

Xiao Xiao, Long Fangyi, Yu Shaolan, Wu Wengjuan, Nie Dayan, Ren Xiaoyan, Li Wen, Wang Xujuan, Yu Ling, Wang Pinghan, Wang Gang

机构信息

Department of Gynecology, Sichuan Provincial Women's and Children's Hospital, The Affiliated Women's and Children's Hospital of Chengdu Medical College, Chengdu, Sichuan, China.

Laboratory Medicine Center, Sichuan Provincial Women's and Children's Hospital, The Affiliated Women's and Children's Hospital of Chengdu Medical College, Chengdu, Sichuan, China.

出版信息

Front Immunol. 2025 Jan 8;15:1496090. doi: 10.3389/fimmu.2024.1496090. eCollection 2024.

DOI:10.3389/fimmu.2024.1496090
PMID:39845977
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11750837/
Abstract

BACKGROUNDS

Collagen type I alpha 1 chain (COL1A1) is a key protein encoding fibrillar collagen, playing a crucial role in the tumor microenvironment (TME) due to its complex functions and close association with tumor invasiveness. This has made COL1A1 a focal point in cancer biology research. However, studies investigating the relationship between COL1A1 expression levels and clinical characteristics of ovarian cancer (OC) remain limited.

METHODS

This study integrated resources from publicly available online databases and immunohistochemistry (IHC) techniques to analyze and validate COL1A1 expression in OC tissues, and evaluated its potential association with clinical features in OC patients. The prognostic value of COL1A1 was assessed using Kaplan-Meier (KM) survival curve analysis. The TIMER and TISIDB databases to explore the potential relationship between COL1A1 expression and immune microenvironment in OC tissues. The LinkedOmics and INPUT2 databases were used to analyze differential gene expression in OC, This was followed by enrichment analysis using the Kyoto Encyclopedia of Genes and Genomes (KEGG) and Gene Ontology (GO) annotations to identify and predict potential signaling pathways associated with COL1A1.

RESULTS

Our study demonstrated that COL1A1 expression was significantly elevated in OC tissues compared to normal ovarian tissues. This elevated expression was closely associated with tumor metastasis, poor prognosis, and advanced pathological stages in OC patients. Moreover, COL1A1 expression showed a significant correlation with immune cell infiltration and the expression of immune-related genes within the TME.Further analyses revealed that COL1A1 and its co-expressed genes were primarily enriched in key signaling pathways involved in OC invasion, metastasis, and angiogenesis, indicating its potential role in driving OC progression.

CONCLUSIONS

Our study found that upregulation of COL1A1 expression is significantly associated with lymph node metastasis of OC and can affect the immune microenvironment. Based on this, COL1A1 could serve as a promising biomarker for OC prognosis and provide a new perspective for the development of potential immunotherapies for patients with OC.

摘要

背景

I型胶原蛋白α1链(COL1A1)是一种编码纤维状胶原蛋白的关键蛋白,因其复杂的功能以及与肿瘤侵袭性的密切关联,在肿瘤微环境(TME)中发挥着至关重要的作用。这使得COL1A1成为癌症生物学研究的焦点。然而,关于COL1A1表达水平与卵巢癌(OC)临床特征之间关系的研究仍然有限。

方法

本研究整合了来自公开在线数据库的资源和免疫组织化学(IHC)技术,以分析和验证OC组织中COL1A1的表达,并评估其与OC患者临床特征的潜在关联。使用Kaplan-Meier(KM)生存曲线分析评估COL1A1的预后价值。利用TIMER和TISIDB数据库探索COL1A1表达与OC组织免疫微环境之间的潜在关系。使用LinkedOmics和INPUT2数据库分析OC中的差异基因表达,随后使用京都基因与基因组百科全书(KEGG)和基因本体论(GO)注释进行富集分析,以识别和预测与COL1A1相关的潜在信号通路。

结果

我们的研究表明,与正常卵巢组织相比,OC组织中COL1A1的表达显著升高。这种升高的表达与OC患者的肿瘤转移、预后不良和晚期病理阶段密切相关。此外,COL1A1表达与TME内的免疫细胞浸润和免疫相关基因的表达显著相关。进一步分析表明,COL1A1及其共表达基因主要富集于参与OC侵袭、转移和血管生成的关键信号通路,表明其在推动OC进展中的潜在作用。

结论

我们的研究发现,COL1A1表达上调与OC的淋巴结转移显著相关,并可影响免疫微环境。基于此,COL1A1有望成为OC预后的生物标志物,并为OC患者潜在免疫治疗的开发提供新的视角。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d3ff/11750837/040451ca47a0/fimmu-15-1496090-g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d3ff/11750837/f5d2e270807a/fimmu-15-1496090-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d3ff/11750837/fae010844b43/fimmu-15-1496090-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d3ff/11750837/883e13b6d4d1/fimmu-15-1496090-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d3ff/11750837/535647d7184f/fimmu-15-1496090-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d3ff/11750837/e21a628b5391/fimmu-15-1496090-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d3ff/11750837/7500531f89aa/fimmu-15-1496090-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d3ff/11750837/cee206209825/fimmu-15-1496090-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d3ff/11750837/df233af7f072/fimmu-15-1496090-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d3ff/11750837/040451ca47a0/fimmu-15-1496090-g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d3ff/11750837/f5d2e270807a/fimmu-15-1496090-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d3ff/11750837/fae010844b43/fimmu-15-1496090-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d3ff/11750837/883e13b6d4d1/fimmu-15-1496090-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d3ff/11750837/535647d7184f/fimmu-15-1496090-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d3ff/11750837/e21a628b5391/fimmu-15-1496090-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d3ff/11750837/7500531f89aa/fimmu-15-1496090-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d3ff/11750837/cee206209825/fimmu-15-1496090-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d3ff/11750837/df233af7f072/fimmu-15-1496090-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d3ff/11750837/040451ca47a0/fimmu-15-1496090-g009.jpg

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