IL-17A Levels in the Sera of Patients with Gastric Cancer Show Limited Elevation

Malek-Hosseini, Zahra; Taherinejad, Marziye; Malekzadeh, Mahyar; Ghaderi, Abbas; Doroudchi, Mehrnoosh

doi:10.7314/apjcp.2015.16.16.7149

Cited by 9 publications

(6 citation statements)

References 40 publications

(47 reference statements)

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“…We believe that these discrepancies may be potentially explained by the different profiles of patients with gastric carcinoma included in the analyses. In the studies in which the authors observed significant increases in systemic IL-17 levels, the majority of the recruited patients with gastric carcinoma were diagnosed with early (I/II TNM) stages of the disease, while in our study as well as in the study by Malek-Hosseini et al 30,. over 60% of patients presented with more advanced disease.…”

Section: Discussionsupporting

confidence: 58%

Interleukins 17 and 23 in patients with gastric neoplasms

Błogowski

Madej-Michniewicz

Marczuk

et al. 2016

Sci Rep

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Recently there has been heightened interest in the potential significance of interleukin (IL)-17 and IL-23 in the development/progression of human malignancies. Here, we analyzed the systemic levels of these cytokines in 75 patients with different types of gastric neoplasms (carcinoma, gastrointestinal stromal tumors, neuroendocrine neoplasms, and lymphomas) and 42 healthy volunteers. We found that patients with all types of gastric neoplasms have significantly lower IL-23 levels. However, in comparison to the levels in healthy individuals, IL-17 concentrations were lower only in patients with types of gastric neoplasms other than carcinoma. Interestingly, IL-17 levels significantly differed between patients with early and advanced gastric carcinoma. No significant associations were detected between the systemic levels of examined interleukins and TNM staging. However, peripheral levels of IL-23 were correlated with the absolute numbers of circulating populations of bone marrow-derived mesenchymal and very small embryonic/epiblast-like stem cells in patients with gastric carcinoma. ROC curve analyses demonstrated that systemic levels of IL-17 seem to meet basic criteria for consideration as a helpful diagnostic marker in the detection of gastric carcinoma. In conclusion, our study provides translational evidence confirming the clinical significance of IL-17 and IL-23 in the pathogenesis of different types of gastric neoplasms in humans.

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Section: Discussionsupporting

confidence: 58%

Interleukins 17 and 23 in patients with gastric neoplasms

Błogowski

Madej-Michniewicz

Marczuk

et al. 2016

Sci Rep

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“…Several human clinical studies have established a relationship between the expression of IL-17A and GC progression. Upregulation of IL-17A is observed in serum and tumor samples of GC patients compared to healthy controls [17][18][19][20][21]. In the present study, IL-17A protein was detectable in the surface mucous epithelium and gastric glands of a normal WT mouse stomach.…”

Section: Discussionsupporting

confidence: 55%

“…Previous studies have shown higher levels of IL-17A in serum and cancer tissues of patients with GC compared with healthy controls [15][16][17][18][19]. Moreover, elevated IL-17A expression in gastric mucosa of mice infected with H. pylori has been reported [24].…”

Section: Il-17a Depletion Suppresses Development Of H Pylori-induced Gcmentioning

confidence: 97%

“…Moreover, expression of IL-17A is significantly increased in tumors of GC patients relative to adjacent nontumor gastric mucosa [15,16]. Increased expression of IL-17A has additionally been reported in sera of GC patients compared to healthy controls [17][18][19]. However, studies to date on the role of IL-17A in GC development have generated inconsistent findings.…”

Section: Introductionmentioning

confidence: 99%

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IL-17A promotes Helicobacter pylori-induced gastric carcinogenesis via interactions with IL-17RC

et al. 2022

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Background Gastric cancer (GC) is a common malignancy worldwide, with a major attribution to Helicobacter pylori. Interleukin (IL)-17A has been reported to be up-regulated in serum and tumor of GC patients, but the precise mechanisms underlying its involvement in gastric tumorigenesis are yet to be established. Here, we investigated the roles of IL-17A in the pathogenesis of H. pylori-induced GC. Methods GC was induced in IL-17A knockout (KO) and wild-type (WT) mice via N-methyl-N-nitrosourea (MNU) treatment and H. pylori infection. At 50 weeks after treatment, gastric tissues were examined by histopathology, immunohistochemistry, and immunoblot analyses. In vitro experiments on the human GC cell lines were additionally performed to elucidate the underlying mechanisms. Results Deletion of IL-17A suppressed MNU and H. pylori-induced gastric tumor development accompanied by a decrease in gastric epithelial cell growth, oxidative stress, and expression of gastric epithelial stem cells markers. In AGS cells, recombinant human IL-17A (rhIL-17A) inhibited apoptosis and G1/S phase transition arrest while promoting reactive oxygen species production, sphere formation ability of cancer stem cells (CSC), and expression of stemness-related genes. In addition, rhIL-17A induced expression of IL-17RC, leading to NF-κB activation and increased NADPH oxidase 1 (NOX1) levels. Inhibition of NOX1 with GKT136901 attenuated rhIL-17A-mediated elevation of GC cell growth, ROS generation, and CSC stemness. Clinically, IL-17RC expressions were significantly upregulated in human GC compared with normal gastric tissues. Conclusion Our results suggest that IL-17A promotes gastric carcinogenesis, in part, by regulating IL-17RC/NF-κB/NOX1 pathway, supporting its potential as a target in human GC therapy.

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“…IL-17 plays a potent role in T-cell mediated angiogenesis, promotes carcinogenesis and it has effects on immune resistance, proliferation and metastasis. IL-17 is predominantly produced and secreted by activated CD4 Tcells [12] It should be noted that IL-17 is also produced by other sources such as natural killer cells (NK), CD8+ T cells, neutrophils, eosinophils, macrophages, dendritic cells and gamma delta T cells (γδT) [13,14]. Regulatory T (Treg) cells, generally known as immune suppressors, also produce IL-17 [15].…”

Section: Introductionmentioning

confidence: 99%

IL-17 (gene expression) as a new biological marker for diagnosing the gastric and colorectal cancer

Rasheed

Alabassi

2022

ijhs

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Background: Malignant gastrointestinal tumors such as esophageal, gastric, liver, colorectal, and pancreatic carcinomas are a major cause of cancer-related deaths worldwide proinflammatory cytokine interleukin-17 (IL-17) produced by Th17 cells, a T helper cell subset developed from an activated CD4+ T cell. IL-17 plays a potent role in T-cell mediated angiogenesis, promotes carcinogenesis and it has effects on immune resistance, proliferation and metastasis. This study was aimed to investicate the Serum IL-17 levels in Iraqi patients with GC and CRC. Materials and methods: peripheral Blood samples were collected from 30 Iraqi patient divided in to two groups 14women and 16 men with age rang 37-57 years, thay attended Gastroenterology and liver teaching hospital in Baghdad city and diagnosed with early detected (early onest) GC and CRC, and 30 healthy women and men were matched with patients as a control. IL-17 serum levels were measured using the highly sensitive Elisa kits (Human IL-17A Mini ABTS ELISA Development Kit , USA) Results:. Elisa assay demonstrated that IL-17 levels were highly expressed in GC and CRC patients, more especially in patients with early detected (early onset) disease.

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IL-17A Levels in the Sera of Patients with Gastric Cancer Show Limited Elevation

Cited by 9 publications

References 40 publications

Interleukins 17 and 23 in patients with gastric neoplasms

Interleukins 17 and 23 in patients with gastric neoplasms

IL-17A promotes Helicobacter pylori-induced gastric carcinogenesis via interactions with IL-17RC

IL-17 (gene expression) as a new biological marker for diagnosing the gastric and colorectal cancer

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