Bioinformatics Analysis of VIPR2 as A Biomarker for Immune Infiltration and Prognosis in Esophageal Adenocarcinoma
10.3971/j.issn.1000-8578.2026.25.0871
- VernacularTitle:VIPR2作为食管腺癌免疫浸润及预后生物标志物的生物信息学分析
- Author:
Ke ZHAO
1
;
Lei LIU
1
;
Guige WANG
1
;
Jiaqi ZHANG
1
;
Libing YANG
1
;
Chao GUO
1
;
Cheng HUANG
1
;
Yeye CHEN
1
;
Shanqing LI
1
Author Information
1. Department of Thoracic Surgery, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing 100730, China.
- Publication Type:SPECIALFEATURE
- Keywords:
Esophageal adenocarcinoma;
VIPR2;
Immune infiltration;
Biomarker;
Prognosis;
Bioinformatics
- From:
Cancer Research on Prevention and Treatment
2026;53(6):430-439
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the expression characteristics, prognostic value, and correlation with immune infiltration of vasoactive intestinal peptide receptor 2 (VIPR2) in esophageal adenocarcinoma (ESAD). Methods Transcriptome data of 80 ESAD and 10 normal tissues were retrieved from the TCGA database. Immune-related differential genes were identified by integrating the ImmPort database. Cox regression analysis was applied to evaluate the prognostic significance of VIPR2. GSVA and ssGSEA were employed to assess the association between VIPR2 and immune-cell infiltration. Functional enrichment was performed using GO, KEGG, and GSEA. Results VIPR2 expression was significantly downregulated in ESAD tissues (P<0.05). High VIPR2 expression was associated with prolonged overall survival (HR=0.246, P=0.047), serving as an independent prognostic factor. Fifteen immune-cell types, including CD8+ T cells, NK cells, and dendritic cells, showed significantly higher infiltration in the VIPR2-high group, whereas Th17-cell abundance was decreased (P<0.05). Enrichment analyses revealed that VIPR2 participated in multiple tumor-immune pathways and was positively correlated with PD-1 and CTLA-4 expression (P<0.01). Conclusion VIPR2 may serve as a potential biomarker in the prognostic assessment and could modulate the tumor-immune microenvironment in ESAD.
