Runan Zhang, Haizhou Wang, Jun Xiao, Jie Lu, Menglin Li, You Zhou, He Sun, Lan Liu, Tizheng Huang, Qiu Zhao
{"title":"<i>CAV1</i> Impacts the Tumor Immune Microenvironment and Has Potential Value of Predicting Response to Immunotherapy in Esophageal Cancer.","authors":"Runan Zhang, Haizhou Wang, Jun Xiao, Jie Lu, Menglin Li, You Zhou, He Sun, Lan Liu, Tizheng Huang, Qiu Zhao","doi":"10.1089/dna.2022.0025","DOIUrl":null,"url":null,"abstract":"<p><p>Caveolin-1 (<i>CAV1</i>) is one of the members of the caveolae, and the role of <i>CAV1</i> in esophageal cancer (ESCA) is not completely clear. In this study, we found that expression of <i>CAV1</i> was downregulated in ESCA in The Cancer Genome Atlas and the Genotype-Tissue Expression (GTEx) database and we also use immunohistochemistry of tissue microarray for verification. Then, we used bioinformatics methods to investigate the prognostic value of <i>CAV1</i>, influence on immune cell infiltration in tumor microenvironment (TME) and responding to immunotherapy in ESCA. Our result indicated that <i>CAV1</i> designs an inflamed TME in ESCA based on the evidence that <i>CAV1</i> positively correlated with immunomodulators, immune score, stomal score, cancer immunity cycles, tumor-infiltrating immune cells, T cell inflamed score, and immune checkpoints. Immunophenoscore, Tumor Immune Dysfunction and Exclusion algorithms, and the mutation analysis show that the downregulated <i>CAV1</i> expression indicated higher tumor mutation burden and higher rate of response to immune checkpoint inhibitors (ICIs) in the low-expression group. In a word, our study demonstrated the impact of <i>CAV1</i> to the TME in ESCA and it may be a new target for ESCA immunotherapy. In addition, the expression of <i>CAV1</i> can predict the clinical response to ICIs, which may provide clinical treatment guidance.</p>","PeriodicalId":11248,"journal":{"name":"DNA and cell biology","volume":"42 1","pages":"27-42"},"PeriodicalIF":2.6000,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"DNA and cell biology","FirstCategoryId":"99","ListUrlMain":"https://doi.org/10.1089/dna.2022.0025","RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q3","JCRName":"BIOCHEMISTRY & MOLECULAR BIOLOGY","Score":null,"Total":0}
引用次数: 0
Abstract
Caveolin-1 (CAV1) is one of the members of the caveolae, and the role of CAV1 in esophageal cancer (ESCA) is not completely clear. In this study, we found that expression of CAV1 was downregulated in ESCA in The Cancer Genome Atlas and the Genotype-Tissue Expression (GTEx) database and we also use immunohistochemistry of tissue microarray for verification. Then, we used bioinformatics methods to investigate the prognostic value of CAV1, influence on immune cell infiltration in tumor microenvironment (TME) and responding to immunotherapy in ESCA. Our result indicated that CAV1 designs an inflamed TME in ESCA based on the evidence that CAV1 positively correlated with immunomodulators, immune score, stomal score, cancer immunity cycles, tumor-infiltrating immune cells, T cell inflamed score, and immune checkpoints. Immunophenoscore, Tumor Immune Dysfunction and Exclusion algorithms, and the mutation analysis show that the downregulated CAV1 expression indicated higher tumor mutation burden and higher rate of response to immune checkpoint inhibitors (ICIs) in the low-expression group. In a word, our study demonstrated the impact of CAV1 to the TME in ESCA and it may be a new target for ESCA immunotherapy. In addition, the expression of CAV1 can predict the clinical response to ICIs, which may provide clinical treatment guidance.
期刊介绍:
DNA and Cell Biology delivers authoritative, peer-reviewed research on all aspects of molecular and cellular biology, with a unique focus on combining mechanistic and clinical studies to drive the field forward.
DNA and Cell Biology coverage includes:
Gene Structure, Function, and Regulation
Gene regulation
Molecular mechanisms of cell activation
Mechanisms of transcriptional, translational, or epigenetic control of gene expression
Molecular Medicine
Molecular pathogenesis
Genetic approaches to cancer and autoimmune diseases
Translational studies in cell and molecular biology
Cellular Organelles
Autophagy
Apoptosis
P bodies
Peroxisosomes
Protein Biosynthesis and Degradation
Regulation of protein synthesis
Post-translational modifications
Control of degradation
Cell-Autonomous Inflammation and Host Cell Response to Infection
Responses to cytokines and other physiological mediators
Evasive pathways of pathogens.