Interaction with neutrophils promotes gastric cancer cell migration and invasion by inducing epithelial-mesenchymal transition

Zhang, Wen; Gu, Jianmei; Chen, Jingyan; Zhang, Peng; Ji, Runbi; Qian, Hui; Xu, Wenrong; Zhang, Xu

doi:10.3892/or.2017.5942

Cited by 59 publications

(42 citation statements)

References 23 publications

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“…In a gastric cancer microenvironment, macrophages via interaction with mesenchymal stem cells induce differentiation of cancer-associated fibroblasts (CAFs) [232][233][234]. CAFs are crucial in the initiation, growth, and migration properties of gastric cancer cells [235,236]. They are responsible for the release of carcinogenic and proinflammatory factors including interleukin-6 (Il-6), cyclooxygenase-2 (COX-2), chemokine (C-X-C motif) ligand 1 (Cxcl1), chemokine (C-X-C motif) ligand 9 (Cxcl9), interferon gamma-induced protein 10 (Cxcl10), stromal cell-derived factor 1 (Cxcl12), and fibroblast-specific protein 1 (FSP1), which promote the EMT process and induce carcinogenesis, promoting migration and invasion [237][238][239].…”

Section: Cancer-associated Fibroblastsmentioning

confidence: 99%

Mechanisms of the Epithelial–Mesenchymal Transition and Tumor Microenvironment in Helicobacter pylori-Induced Gastric Cancer

Baj

Korona-Głowniak

Forma

et al. 2020

Cells

124

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Helicobacter pylori (H. pylori) is one of the most common human pathogens, affecting half of the world's population. Approximately 20% of the infected patients develop gastric ulcers or neoplastic changes in the gastric stroma. An infection also leads to the progression of epithelial-mesenchymal transition within gastric tissue, increasing the probability of gastric cancer development. This paper aims to review the role of H. pylori and its virulence factors in epithelial-mesenchymal transition associated with malignant transformation within the gastric stroma. The reviewed factors included: CagA (cytotoxin-associated gene A) along with induction of cancer stem-cell properties and interaction with YAP (Yes-associated protein pathway), tumor necrosis factor α-inducing protein, Lpp20 lipoprotein, Afadin protein, penicillin-binding protein 1A, microRNA-29a-3p, programmed cell death protein 4, lysosomal-associated protein transmembrane 4β, cancer-associated fibroblasts, heparin-binding epidermal growth factor (HB-EGF), matrix metalloproteinase-7 (MMP-7), and cancer stem cells (CSCs). The review summarizes the most recent findings, providing insight into potential molecular targets and new treatment strategies for gastric cancer.

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Section: Cancer-associated Fibroblastsmentioning

confidence: 99%

Mechanisms of the Epithelial–Mesenchymal Transition and Tumor Microenvironment in Helicobacter pylori-Induced Gastric Cancer

Baj

Korona-Głowniak

Forma

et al. 2020

Cells

124

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“…In this study, infiltration of plasma cells was also shown to prolong survival in gastric cancer as a component of the humoral immune response, consistent with previous studies (18,19); however, the precise role of these cells remains poorly understood. Neutrophils were assigned the highest coefficient in our risk assessment formula, possibly due to their ability to regulate many of the malignancy-associated behaviors of cancer cells, such as migration and invasion (20,21). The difference in infiltration ratio among these four immune cell types may be correlated with leukocyte migration-related pathways, which were enriched in our high risk subgroup; a high risk score was indicative of infiltrates with a high proportion of neutrophils and low proportions of plasma cells, activated CD4 + memory T cells, and Tfh cells.…”

Section: Discussionmentioning

confidence: 99%

Tumor-Infiltrating Lymphocyte-Based Risk Score for Predicting Prognosis in Gastric Cancer

Xie

et al. 2020

Front. Oncol.

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Tumor-infiltrating lymphocytes (TILs) in gastric cancer are closely related to clinical prognosis; however, little is known regarding the immune microenvironment in this disease. Thus, RNA-sequencing data from gastric cancer patients were downloaded from the Gene Expression Omnibus (GEO). The proportion of immune cells was determined based on a deconvolution algorithm (CIBERSORT), and gene expression profiles were analyzed in the context of clinical outcomes to construct an immune risk score. Data were analyzed using least absolute shrinkage and selection operator (LASSO) and multivariable Cox regression, to identify prognostic markers of gastric cancer survival. The model included four immune cell types: neutrophils, plasma cells, activated CD4 + memory T cells, and T follicular helper cells. Patients were classified into two subgroups based on risk score, and a significant difference in overall survival (OS) was seen between the subgroups in both the training and testing cohorts, particularly in patients with tumor stages ≥T3. Multivariable analysis revealed that both T-stage and risk score were independent prognostic factors for gastric cancer survival [hazard ratio (HR) 1.505; 95% confidence interval (CI) 1.043-2.173, HR 1.686; 95% CI 1.367-2.080]. Risk scores and clinical factors were then integrated into a nomogram to build a model with both good discriminatory power and accuracy in predicting clinical outcomes. Further analysis using gene set enrichment analysis (GSEA) identified strong associations of immune risk with TGF-β and tumor metastasis-related pathways, which could inform research on the molecular mechanisms of gastric cancer. Collectively, the data presented here suggest that an immune risk model can make an important contribution to predictions prognosis in gastric cancer patients.

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“…Neutrophil-cancer cell interaction can lead to the polarization of neutrophils towards a pro-tumor phenotype [101]. found that bone marrow neutrophils in mice activated by GC cells promote their ability to migrate, thus leading to increased invasiveness.…”

Section: Bone Marrow Neutrophilsmentioning

confidence: 99%

“…Cancer-associated fibroblasts (CAFs) have been shown to have a crucial influence on the initiation, growth, and migration of tumor cells [101]. This is especially due to the reduced cell-to-cell adhesion, enhanced mobility, and constant activation [87,105].…”

Section: Cancer-associated Fibroblastsmentioning

confidence: 99%

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Immunological Aspects of the Tumor Microenvironment and Epithelial-Mesenchymal Transition in Gastric Carcinogenesis

Baj

Brzozowska

Forma

et al. 2020

IJMS

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Infection with Helicobacter pylori, a Gram-negative, microaerophilic pathogen often results in gastric cancer in a subset of affected individuals. This explains why H. pylori is the only bacterium classified as a class I carcinogen by the World Health Organization. Several studies have pinpointed mechanisms by which H. pylori alters signaling pathways in the host cell to cause diseases. In this article, the authors have reviewed 234 studies conducted over a span of 18 years (2002)(2003)(2004)(2005)(2006)(2007)(2008)(2009)(2010)(2011)(2012)(2013)(2014)(2015)(2016)(2017)(2018)(2019)(2020). The studies investigated the various mechanisms associated with gastric cancer induction. For the past 1.5 years, researchers have discovered new mechanisms contributing to gastric cancer linked to H. pylori etiology. Alongside alteration of the host signaling pathways using oncogenic CagA pathways, H. pylori induce DNA damage in the host and alter the methylation of DNA as a means of perturbing downstream signaling. Also, with H. pylori, several pathways in the host cell are activated, resulting in epithelial-to-mesenchymal transition (EMT), together with the induction of cell proliferation and survival. Studies have shown that H. pylori enhances gastric carcinogenesis via a multifactorial approach. What is intriguing is that most of the targeted mechanisms and pathways appear common with various forms of cancer.EMT refers to the process by which the mesenchymal phenotype is acquired by epithelial cells (ECs) mainly via the reduction of their intracellular adhesions and proliferative capacity (Figure 1.) [47].

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Interaction with neutrophils promotes gastric cancer cell migration and invasion by inducing epithelial-mesenchymal transition

Cited by 59 publications

References 23 publications

Mechanisms of the Epithelial–Mesenchymal Transition and Tumor Microenvironment in Helicobacter pylori-Induced Gastric Cancer

Mechanisms of the Epithelial–Mesenchymal Transition and Tumor Microenvironment in Helicobacter pylori-Induced Gastric Cancer

Tumor-Infiltrating Lymphocyte-Based Risk Score for Predicting Prognosis in Gastric Cancer

Immunological Aspects of the Tumor Microenvironment and Epithelial-Mesenchymal Transition in Gastric Carcinogenesis

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