Comprehensive analysis of the expression, prognostic, and immune infiltration for COL4s in stomach adenocarcinoma.


Journal

BMC medical genomics
ISSN: 1755-8794
Titre abrégé: BMC Med Genomics
Pays: England
ID NLM: 101319628

Informations de publication

Date de publication:
21 Jun 2024
Historique:
received: 08 06 2023
accepted: 14 06 2024
medline: 22 6 2024
pubmed: 22 6 2024
entrez: 21 6 2024
Statut: epublish

Résumé

Collagen (COL) genes, play a key role in tumor invasion and metastasis, are involved in tumor extracellular matrix (ECM)-receptor interactions and focal adhesion pathways. However, studies focusing on the diagnostic value of the COL4 family in stomach adenocarcinoma (STAD) are currently lacking. The TCGA database was employed to retrieve the clinical features and RNA sequencing expression profiles of patients with STAD. We conducted an investigation to examine the expression disparities between STAD and adjacent normal tissues. Kaplan-Meier survival analysis was utilized to assess their prognostic significance, while Spearman correlation analysis was employed to determine their association with immune checkpoint genes and immunomodulatory molecules. Furthermore, GO and KEGG analyses were performed on the COL4s-related genes, revealing potential biological pathways through gene set enrichment analysis (GSEA). Subsequently, we explored the extent of immune infiltration of the COL4 family in STAD using the TIMER database. Lastly, the expression levels of the COL4 family in STAD were further validated through quantitative PCR (qPCR) and western blot techniques. The expression levels of COL4A1/2 were significantly upregulated, while COL4A5/6 were conspicuously downregulated in STAD. The survival analysis revealed that the upregulated COL4s indicated poorer overall survival, first progression and post-progression survival outcomes. Additionally, our findings demonstrated a positive correlation between the expressions of COL4A1/2/3/4 and the infiltration of immune cells, including CD8 + T cells, dendritic cells, macrophages, neutrophils and CD4 + T cells. Further correlation analysis uncovered a favorable association between the expression of COL4A1/2/3/4 and various crucial immunomodulatory molecules, immunological checkpoint molecules, and chemokines. Quantitative PCR analysis confirmed that the expression patterns of COL4A1/3/4/6 genes aligned with the finding from the TCGA database. However, gastric cancer cells exhibited downregulation of COL4A2. Consistently, the protein level of COL4A1 was elevated, whereas the protein level of COL4A2 was reduced in the gastric cancer cell lines. COL4s could potentially serve as biomarkers for diagnosing and predicting the prognosis of STAD.

Sections du résumé

BACKGROUND BACKGROUND
Collagen (COL) genes, play a key role in tumor invasion and metastasis, are involved in tumor extracellular matrix (ECM)-receptor interactions and focal adhesion pathways. However, studies focusing on the diagnostic value of the COL4 family in stomach adenocarcinoma (STAD) are currently lacking.
METHODS METHODS
The TCGA database was employed to retrieve the clinical features and RNA sequencing expression profiles of patients with STAD. We conducted an investigation to examine the expression disparities between STAD and adjacent normal tissues. Kaplan-Meier survival analysis was utilized to assess their prognostic significance, while Spearman correlation analysis was employed to determine their association with immune checkpoint genes and immunomodulatory molecules. Furthermore, GO and KEGG analyses were performed on the COL4s-related genes, revealing potential biological pathways through gene set enrichment analysis (GSEA). Subsequently, we explored the extent of immune infiltration of the COL4 family in STAD using the TIMER database. Lastly, the expression levels of the COL4 family in STAD were further validated through quantitative PCR (qPCR) and western blot techniques.
RESULTS RESULTS
The expression levels of COL4A1/2 were significantly upregulated, while COL4A5/6 were conspicuously downregulated in STAD. The survival analysis revealed that the upregulated COL4s indicated poorer overall survival, first progression and post-progression survival outcomes. Additionally, our findings demonstrated a positive correlation between the expressions of COL4A1/2/3/4 and the infiltration of immune cells, including CD8 + T cells, dendritic cells, macrophages, neutrophils and CD4 + T cells. Further correlation analysis uncovered a favorable association between the expression of COL4A1/2/3/4 and various crucial immunomodulatory molecules, immunological checkpoint molecules, and chemokines. Quantitative PCR analysis confirmed that the expression patterns of COL4A1/3/4/6 genes aligned with the finding from the TCGA database. However, gastric cancer cells exhibited downregulation of COL4A2. Consistently, the protein level of COL4A1 was elevated, whereas the protein level of COL4A2 was reduced in the gastric cancer cell lines.
CONCLUSION CONCLUSIONS
COL4s could potentially serve as biomarkers for diagnosing and predicting the prognosis of STAD.

Identifiants

pubmed: 38907304
doi: 10.1186/s12920-024-01934-3
pii: 10.1186/s12920-024-01934-3
doi:

Substances chimiques

Collagen Type IV 0
Biomarkers, Tumor 0

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

168

Subventions

Organisme : Zhejiang Provincial Natural Science Foundation
ID : LGF21H310004
Organisme : Zhejiang Provincial Natural Science Foundation
ID : LY21H270013
Organisme : Zhejiang Medical and Health Science and Technology Plan
ID : WKJ-ZJ-2136
Organisme : Key R&D Program of Zhejiang Province
ID : 2023C03054
Organisme : Key R&D Program of Zhejiang Province
ID : 2024C03048
Organisme : Hangzhou Medical and Health Science and Technology Plan
ID : 2016ZD01
Organisme : Medical and Health Technology Plan Project of Hangzhou
ID : Z20230039

Informations de copyright

© 2024. The Author(s).

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Auteurs

Ying Xu (Y)

Department of Gastroenterology, Affiliated Hangzhou First People's Hospital, Westlake University School of Medicine, Hangzhou, China.
Hangzhou Institute of Digestive Diseases, Hangzhou, China.
Key Laboratory of Integrated Traditional Chinese and Western Medicine for Biliary and Pancreatic Diseases of Zhejiang Province, Hangzhou, China.

Hangbin Jin (H)

Department of Gastroenterology, Affiliated Hangzhou First People's Hospital, Westlake University School of Medicine, Hangzhou, China.
Hangzhou Institute of Digestive Diseases, Hangzhou, China.
Key Laboratory of Integrated Traditional Chinese and Western Medicine for Biliary and Pancreatic Diseases of Zhejiang Province, Hangzhou, China.
Key Laboratory of Clinical Cancer Pharmacology and Toxicology Research of Zhejiang Province, Hangzhou, Zhejiang, China.

Yan Chen (Y)

Department of Gastroenterology, Affiliated Hangzhou First People's Hospital, Westlake University School of Medicine, Hangzhou, China.
Hangzhou Institute of Digestive Diseases, Hangzhou, China.
Key Laboratory of Integrated Traditional Chinese and Western Medicine for Biliary and Pancreatic Diseases of Zhejiang Province, Hangzhou, China.

Zhen Yang (Z)

School of Life Sciences, Zhejiang Chinese Medical University, Hangzhou, China.

Dongchao Xu (D)

Department of Gastroenterology, Affiliated Hangzhou First People's Hospital, Westlake University School of Medicine, Hangzhou, China.
Hangzhou Institute of Digestive Diseases, Hangzhou, China.
Key Laboratory of Integrated Traditional Chinese and Western Medicine for Biliary and Pancreatic Diseases of Zhejiang Province, Hangzhou, China.

Xiaofeng Zhang (X)

Department of Gastroenterology, Affiliated Hangzhou First People's Hospital, Westlake University School of Medicine, Hangzhou, China. zhangxiaofeng837@163.com.
Hangzhou Institute of Digestive Diseases, Hangzhou, China. zhangxiaofeng837@163.com.
Key Laboratory of Integrated Traditional Chinese and Western Medicine for Biliary and Pancreatic Diseases of Zhejiang Province, Hangzhou, China. zhangxiaofeng837@163.com.
Key Laboratory of Clinical Cancer Pharmacology and Toxicology Research of Zhejiang Province, Hangzhou, Zhejiang, China. zhangxiaofeng837@163.com.

Jianfeng Yang (J)

Department of Gastroenterology, Affiliated Hangzhou First People's Hospital, Westlake University School of Medicine, Hangzhou, China. yjf-1976@163.com.
Hangzhou Institute of Digestive Diseases, Hangzhou, China. yjf-1976@163.com.
Key Laboratory of Integrated Traditional Chinese and Western Medicine for Biliary and Pancreatic Diseases of Zhejiang Province, Hangzhou, China. yjf-1976@163.com.
Key Laboratory of Clinical Cancer Pharmacology and Toxicology Research of Zhejiang Province, Hangzhou, Zhejiang, China. yjf-1976@163.com.

Yu Wang (Y)

Department of Gastroenterology, Affiliated Hangzhou First People's Hospital, Westlake University School of Medicine, Hangzhou, China. wangyu@zcmu.edu.cn.
Hangzhou Institute of Digestive Diseases, Hangzhou, China. wangyu@zcmu.edu.cn.
Key Laboratory of Integrated Traditional Chinese and Western Medicine for Biliary and Pancreatic Diseases of Zhejiang Province, Hangzhou, China. wangyu@zcmu.edu.cn.

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