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      Association between rs3761548 polymorphism of FOXP3 and the risk of gastric cancer: a case-control study

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          Abstract

          Gastric cancer is one of the most prevalent malignancies in the world. Various factors play a role in the development of this disease as risk factors. One of these genes is the FOXP3, which is located on the short arm of the X chromosome (Xp11.23). The rs3761548 polymorphism in the promoter region of this gene increases cell proliferation. In the current study, the association between this genetic polymorphism and the risk of gastric cancer was investigated. This study included 147 patients (55 women, 92 men) with gastric cancer and 147 healthy individuals (53 women, 94 men). The PCR-RFLP method is used for genotyping. Statistical analysis showed that there was no significant association between this polymorphism and the risk of gastric cancer. However, the analysis of genotype, family history and smoking risk factors simultane-oussly revealed a significant relationship between simultaneous occurrence of two (OR=3.79, 95% CI=1.77-8.09, p=0.001) and three risk factors (OR=6.44, 95% CI=1.76-23.5, p=0.017) and the risk of gastric cancer.

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          IL-2 regulates FOXP3 expression in human CD4+CD25+ regulatory T cells through a STAT-dependent mechanism and induces the expansion of these cells in vivo.

          Emmanuel Zorn, Erik A. Nelson, Mehrdad Mohseni … (2006)
          IL-2 plays a critical role in the maintenance of CD4+CD25+ FOXP3(+) regulatory T cells (Tregs) in vivo. We examined the effects of IL-2 signaling in human Tregs. In vitro, IL-2 selectively up-regulated the expression of FOXP3 in purified CD4+CD25+ T cells but not in CD4+CD25- cells. This regulation involved the binding of STAT3 and STAT5 proteins to a highly conserved STAT-binding site located in the first intron of the FOXP3 gene. We also examined the effects of low-dose IL-2 treatment in 12 patients with metastatic cancer and 9 patients with chronic myelogenous leukemia after allogeneic hematopoietic stem cell transplantation. Overall, IL-2 treatment resulted in a 1.9 median fold increase in the frequency of CD4+CD25+ cells in peripheral blood as well as a 9.7 median fold increase in FOXP3 expression in CD3+ T cells. CD56+CD3- natural killer (NK) cells also expanded during IL-2 therapy but did not express FOXP3. In vitro treatment of NK cells with 5-aza-2'-deoxycytidine restored the IL-2 signaling pathway leading to FOXP3 expression, suggesting that this gene was constitutively repressed by DNA methylation in these cells. Our findings support the clinical evaluation of low-dose IL-2 to selectively modulate CD4+CD25+ Tregs and increase expression of FOXP3 in vivo.
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            Mechanisms of regulatory T cell infiltration in tumors: implications for innovative immune precision therapies

            Shohei Koyama, Hiroyoshi Nishikawa (2021)
            With the broad application of cancer immunotherapies such as immune checkpoint inhibitors in multiple cancer types, the immunological landscape in the tumor microenvironment (TME) has become enormously important for determining the optimal cancer treatment. Tumors can be immunologically divided into two categories: inflamed and non-inflamed based on the extent of immune cell infiltration and their activation status. In general, immunotherapies are preferable for the inflamed tumors than for non-inflamed tumors. Regulatory T cells (Tregs), an immunosuppressive subset of CD4 + T cells, play an essential role in maintaining self-tolerance and immunological homeostasis. In tumor immunity, Tregs compromise immune surveillance against cancer in healthy individuals and impair the antitumor immune response in tumor-bearing hosts. Tregs, therefore, accelerate immune evasion by tumor cells, leading to tumor development and progression in various types of cancer. Therefore, Tregs are considered to be a crucial therapeutic target for cancer immunotherapy. Abundant Tregs are observed in the TME in many types of cancer, both in inflamed and non-inflamed tumors. Diverse mechanisms of Treg accumulation, activation, and survival in the TME have been uncovered for different tumor types, indicating the importance of understanding the mechanism of Treg infiltration in each patient when selecting the optimal Treg-targeted therapy. Here, we review recent advances in the understanding of mechanisms leading to Treg abundance in the TME to optimize Treg-targeted therapy. Furthermore, in addition to the conventional strategies targeting cell surface molecules predominantly expressed by Tregs, reagents targeting molecules and signaling pathways specifically employed by Tregs for infiltration, activation, and survival in each tumor type are illustrated as novel Treg-targeted therapies. The effectiveness of immune precision therapy depends on conditions in the TME of each cancer patient.
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              Gastric cancer prevention strategies: a global perspective

              Leonardo Eusebi, Andrea Telese, Giovanni Marasco … (2020)
              Gastric cancer (GC) is the fifth most common cancer worldwide, and mortality rates are still high. Primary preventive strategies, aimed to reduce risk factors and promote protective ones, will lead to a decrease in GC incidence. Helicobacter pylori infection is a well-established carcinogen for GC, and its eradication is recommended as the best strategy for the primary prevention. However, the role of other factors such as lifestyle, diet, and drug use is still under debate in GC carcinogenesis. Unfortunately, most patients with GC are diagnosed at late stages when treatment is often ineffective. Neoplastic transformation of the gastric mucosa is a multistep process, and appropriate diagnosis and management of preneoplastic conditions can reduce GC-related mortality. Several screening strategies in relation to GC incidence have been proposed in order to detect neoplastic lesions at early stages. The efficacy of screening strategies in reducing GC mortality needs to be confirmed. This review provides an overview of current international guidelines and recent literature on primary and secondary prevention strategies for GC.
              Article 0 comments Cited 115 times – based on 0 reviews     Review now
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                Author and article information

                Journal
                Journal ID (nlm-ta): Mol Biol Res Commun
                Journal ID (iso-abbrev): Mol Biol Res Commun
                Journal ID (publisher-id): MBRC
                Title: Molecular Biology Research Communications
                Publisher: Shiraz University (Shiraz, Iran )
                ISSN (Print): 2322-181X
                ISSN (Electronic): 2345-2005
                Publication date (Print): 2024
                Volume: 13
                Issue: 4
                Pages: 247-252
                Affiliations
                [1] Department of Biology, Faculty of Science, Shiraz University, Shiraz, Iran
                Author notes
                [* ]Corresponding Author: Department of Biology, Faculty of Science,Shiraz University, Shiraz, 71467-13565, Iran Tel: +98 71 36 13 7435; Fax: +98 71 32280916; Email: isaadat@shirazu.ac.ir
                Article
                DOI: 10.22099/mbrc.2024.49125.1989
                PMC ID: 11416849
                PubMed ID: 39315286
                SO-VID: 49a67a29-40a1-44c0-aec4-6e6fd69413ed
                License:

                This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( https://creativecommons.org/licenses/by/4.0/)

                History
                Categories
                Subject: Original Article

                Keywords: foxp3,gastric cancer,genetic polymorphisms,pcr-rflp
                Data availability:
                Keywords: foxp3, gastric cancer, genetic polymorphisms, pcr-rflp

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