The Roles of Immune Cells in Gastric Cancer: Anti-Cancer or Pro-Cancer?

Sukri, Asif; Hanafiah, Alfizah; Kosai, Nik Ritza

doi:10.3390/cancers14163922

Cited by 14 publications

(7 citation statements)

References 109 publications

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“…B cells can promote the development of CD4+ effector T cells and memory T cells, whereas T cells are associated with GC prognosis. [ 51 ]…”

Section: Discussionmentioning

confidence: 99%

“…B cells can promote the development of CD4+ effector T cells and memory T cells, whereas T cells are associated with GC prognosis. [51] Molecular alterations in EGC play a crucial role in GC progression and prognosis. [11,13] In this study, three mRNAs (ADGRG7, CT83, and MMP12) associated with EGC were screened to construct a 3-gene prognostic risk model for GC patients by conducting COX and LASSO regression analyses.…”

Section: Discussionmentioning

confidence: 99%

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Quantitative Analysis on Molecular Characteristics Evolution of Gastric Cancer Progression and Prognosis

Wei

et al. 2023

Advanced Biology

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The dynamic changes of key biological characteristics from gastric low‐grade intraepithelial neoplasia (LGIN) to high‐grade intraepithelial neoplasia (HGIN) to early gastric cancer (EGC) are still unclear, which greatly affect the accurate diagnosis and treatment of EGC and prognosis evaluation of gastric cancer (GC). In this study, bioinformatics methods/tools are applied to quantitatively analyze molecular characteristics evolution of GC progression, and a prognosis model is constructed. This study finds that some dysregulated differentially expressed mRNAs (DEmRNAs) in the LGIN stage may continue to promote the occurrence and development of EGC. Among the LGIN, HGIN, and EGC stages, there are differences and relevance in the transcription expression patterns of DEmRNAs, and the activation related to immune cells is very different. The biological functions continuously changed during the progression from LGIN to HGIN to EGC. The COX model constructed based on the three EGC‐related DEmRNAs has GC prognostic risk prediction ability. The evolution of biological characteristics during the development of EGC mined by the authors provides new insight into understanding the molecular mechanism of EGC occurrence and development. The three‐gene prognostic risk model provides a new method for assisting GC clinical treatment decisions.

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“…B cells can promote the development of CD4+ effector T cells and memory T cells, whereas T cells are associated with GC prognosis. [ 51 ]…”

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Quantitative Analysis on Molecular Characteristics Evolution of Gastric Cancer Progression and Prognosis

Wei

et al. 2023

Advanced Biology

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“…Under normal circumstances, B cells, NK cells and other immune cells are involved in the clearance of tumor cells by the immune system, but this requires a sufficient number of immune cells that are functioning properly. 35 , 36 Upregulated immune checkpoint molecules inhibit the activation of immune cells, so oncogenic hub genes may lead to inactivation of immune cells such as B cells, NK cells, and ultimately promote the proliferation of EAC cells.…”

Section: Discussionmentioning

confidence: 99%

Construction of the Interaction Network of Hub Genes in the Progression of Barrett’s Esophagus to Esophageal Adenocarcinoma

Li¹,

Duan²,

He³

et al. 2023

JIR

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Introduction: Esophageal adenocarcinoma (EAC) is one of the histologic types of esophageal cancer with a poor prognosis. The majority of EAC originate from Barrett's esophagus (BE). There are few studies focusing on the dynamic progression of BE to EAC. Methods: R software was used to analyze differentially expressed genes (DEGs) based on RNA-seq data of 94 normal esophageal squamous epithelial (NE) tissues, 113 BE tissues and 147 EAC tissues. The overlapping genes of DEGs between BE and EAC were analyzed by Venn diagram tool. The hub genes were selected by Cytoscape software based on the protein-protein interaction network of the overlapping genes using STRING database. The functional analysis of hub genes was performed by R software and the protein expression was identified by immunohistochemistry. Results: In the present study, we found a large degree of genetic similarity between BE and EAC, and further identified seven hub genes (including COL1A1, TGFBI, MMP1, COL4A1, NID2, MMP12, CXCL1) which were all progressively upregulated in the progression of NE-BE-EAC. We have preliminarily uncovered the probable molecular mechanisms of these hub genes in disease development and constructed the ceRNA regulatory network of hub genes. More importantly, we explored the possibility of hub genes as biomarkers in the disease progression of NE-BE-EAC. For example, TGFBI can be used as biomarkers to predict the prognosis of EAC patients. COL1A1, NID2 and COL4A1 can be used as biomarkers to predict the response to immune checkpoint blockade (ICB) therapy. We also constructed a disease progression risk model for NE-BE-EAC based on CXCL1, MMP1 and TGFBI. Finally, the results of drug sensitivity analysis based on hub genes showed that drugs such as PI3K inhibitor TGX221, bleomycin, PKC inhibitor Midostaurin, Bcr-Abl inhibitor Dasatinib, HSP90 inhibitor 17-AAG, and Docetaxel may be potential candidates to inhibit the progression of BE to EAC. Conclusion:This study is based on a large number of clinical samples with high credibility, which is useful for revealing the probable carcinogenic mechanism of BE to EAC and developing new clinical treatment strategies.

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“…Acting as conductors in the immune orchestra, T helper cells (CD4+) harmonize responses. From catalyzing antibody production to activating macrophages, their multifunctionality extends to orchestrating a cohesive defense, uniting immune forces against gastric and CRCs (19). Additionally, at the heart of adaptive immunity, B cells showcase versatility.…”

Section: Immune Microenvironment In Gi Cancersmentioning

confidence: 99%

Pathways and molecules for overcoming immunotolerance in metastatic gastrointestinal tumors

Gan,

Li,

et al. 2024

Front. Immunol.

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Worldwide, gastrointestinal (GI) cancer is recognized as one of the leading malignancies diagnosed in both genders, with mortality largely attributed to metastatic dissemination. It has been identified that in GI cancer, a variety of signaling pathways and key molecules are modified, leading to the emergence of an immunotolerance phenotype. Such modifications are pivotal in the malignancy’s evasion of immune detection. Thus, a thorough analysis of the pathways and molecules contributing to GI cancer’s immunotolerance is vital for advancing our comprehension and propelling the creation of efficacious pharmacological treatments. In response to this necessity, our review illuminates a selection of groundbreaking cellular signaling pathways associated with immunotolerance in GI cancer, including the Phosphoinositide 3-kinases/Akt, Janus kinase/Signal Transducer and Activator of Transcription 3, Nuclear Factor kappa-light-chain-enhancer of activated B cells, Transforming Growth Factor-beta/Smad, Notch, Programmed Death-1/Programmed Death-Ligand 1, and Wingless and INT-1/beta-catenin-Interleukin 10. Additionally, we examine an array of pertinent molecules like Indoleamine-pyrrole 2,3-dioxygenase, Human Leukocyte Antigen G/E, Glycoprotein A Repetitions Predominant, Clever-1, Interferon regulatory factor 8/Osteopontin, T-cell immunoglobulin and mucin-domain containing-3, Carcinoembryonic antigen-related cell adhesion molecule 1, Cell division control protein 42 homolog, and caspases-1 and -12.

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The Roles of Immune Cells in Gastric Cancer: Anti-Cancer or Pro-Cancer?

Cited by 14 publications

References 109 publications

Quantitative Analysis on Molecular Characteristics Evolution of Gastric Cancer Progression and Prognosis

Quantitative Analysis on Molecular Characteristics Evolution of Gastric Cancer Progression and Prognosis

Construction of the Interaction Network of Hub Genes in the Progression of Barrett’s Esophagus to Esophageal Adenocarcinoma

Pathways and molecules for overcoming immunotolerance in metastatic gastrointestinal tumors

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