MicroRNAs 142-3p, miR-155 and miR-203 Are Deregulated in Gastric MALT Lymphomas Compared to Chronic Gastritis

Fernández, Concepción; Bellosillo, Beatríz; Ferraro, Mariana; Seoane, Agustín; Sánchez‐González, Blanca; Pairet, Silvia; Pons, Aina; Barranco, Luis; Vela, Maria Carmen; Gimeno, Eva; Colomo, Lluı́s; Besses, Carles; Navarro, Alfons; Salar, Antonio

doi:10.21873/cgp.20020

Cited by 25 publications

(28 citation statements)

References 43 publications

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“…They found a significant overexpression of miR‐142‐3p and miR‐155 and downregulation of miR‐203 in GML as compared to gastritis. They suggested that expression levels of miR‐142‐3p, miR‐155, and miR‐203 could be useful biomarkers for the differential diagnosis between GML and gastritis . Similarly, Floch et al.…”

Section: Gastric Mucosa‐associated Lymphoid Tissue (Malt) Lymphomamentioning

confidence: 96%

“…They suggested that expression levels of miR-142-3p, miR-155, and miR-203 could be useful biomarkers for the differential diagnosis between GML and gastritis. 13 Similarly, Floch et al studied regulation of miRNAs in a GML mouse model using BALB/c mice thymectomized at 3 day postbirth (d3Tx model) and infected with H. pylori. They found five miRNAs overexpressed in GML.…”

Section: Gastric Cancer: Biomarkers For Treatment Responsementioning

confidence: 99%

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Helicobacter pylori, gastric cancer and other gastrointestinal malignancies

et al. 2017

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In a retrospective study performed in California, U.S.A., ca. 3% of patients with gastric intestinal metaplasia (GIM) developed gastric cancer (GC) within a median time period of 4.6 years after diagnosis of GIM. This observation stresses the importance of targeted surveillance even in regions with a low GC prevalence. Patients with alcoholic liver disease as well as survivors of colorectal and lobular breast cancer were found to be at increased risk of secondary GC. A population-based Chinese study confirmed "serologic biopsy" as a useful screening tool for stratifying the individual risk of developing GC. Concerning GC therapy, a post hoc analysis of the MAGIC trial reported that regression of lymph node metastases, but not the tumor regression itself, predicts overall survival. Furthermore, in patients with high microsatellite instable tumors, perioperative chemotherapy leads to an increased risk of mortality. Two studies confirmed that eradication therapy is worthwhile as an initial treatment for gastric mucosa-associated lymphoid tissue (MALT) lymphoma irrespective of the H. pylori infection status and stage. An increased risk of a second primary malignancy including GC was observed in these patients treated with immuno/chemotherapy but not in patients treated solely with an H. pylori eradication treatment. With respect to gastrointestinal malignancies other than GC, discrepant data have been published regarding the association of H. pylori with pancreatic cancer whereas no association has been reported with esophageal squamous cell carcinoma. The majority of published studies still support an association of H. pylori with colon neoplasms.

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Section: Gastric Mucosa‐associated Lymphoid Tissue (Malt) Lymphomamentioning

confidence: 96%

Section: Gastric Cancer: Biomarkers For Treatment Responsementioning

confidence: 99%

Helicobacter pylori, gastric cancer and other gastrointestinal malignancies

et al. 2017

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“…miRNA dysregulation has been indicated to induce cancer cell proliferation, inflammation, invasion, migration, and metastasis . Previous studies showed that miR‐155 was involved in GC‐associated inflammation, ie, miR‐155 is expressed by immune cells such as macrophages, dendritic cells, and various subsets of lymphocytes, and it affected both pro‐ and anti‐inflammation in myeloid cells and several cancers . Unfortunately, little is known about miR‐155 in GC.…”

Section: Introductionmentioning

confidence: 99%

Helicobacter pylori CagA promotes the malignant transformation of gastric mucosal epithelial cells through the dysregulation of the miR‐155/KLF4 signaling pathway

Ren

Zhao

et al. 2019

Molecular Carcinogenesis

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The Helicobacter pylori (H. pylori) cytotoxin-associated gene A (CagA) and Krüppel-like transcription factor (KLF4) were both closely associated with the development and progression of gastric cancer (GC). However, the nature of the interactions between CagA and KLF4 in GC development has not been elucidated. Therefore, we focused on the CagA-mediated promotion of the malignant transformation of gastric epithelial cells. Herein, we first examined the expression of KLF4 in both human cancer and paracarcinoma tissues with or without H. pylori infection and found that KLF4 expression was significantly decreased in H. pylori-positive GC cells compared with the H. pylori-negative GC cells. Further functional studies revealed that the increased expression of CagA could suppress KLF4 expression and promote the malignant transformation of normal epithelial cells. Subsequently, we found that CagA could upregulate miR-155 and further restrict the expression of downstream KLF4. More importantly, the overexpression of miR-155 in GES-1 promoted epithelial-mesenchymal transition and eventually facilitated tumor growth in vivo. Overall, the identification of the CagA/miR-155/KLF4 signaling pathway provided a new insight into the development and treatment of GC. K E Y W O R D S CagA, gastric cancer, Helicobacter pylori, Krüppel-like factor 4, miR-155

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“…NF-kB and BCR activation plays a key role in MALT lymphomagenesis [ 23 ]. Former studies have shown the upregulation of miR-142 and miR-155 when comparing human GML tissue to normal mucosa [ 24 ] and chronic gastritis [ 25 ]. Both miR-142 and miR-155 inhibit the pro-apoptoticstress-induced P53 target gene (TP53INP1), thus accelerating MALT lymphoma proliferation [ 23 ].…”

Section: Resultsmentioning

confidence: 99%

“…Fernandez et al proposed the use of the quantitative expression of miR-142-3p and miR-155 to better distinguish between chronic gastritis and gastric MALT lymphoma. Finally, in the disseminate presentation of gastric MALT lymphoma, among 23 miRNAs, miR-142-3p and miR-155 were found to be downregulated [ 25 ]. Several studies about the prognostic value of miR-155 expression have been conducted.…”

Section: Resultsmentioning

confidence: 99%

Involvement of miR-142 and miR-155 in Non-Infectious Complications of CVID

et al. 2020

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Background and objectives: Common variable immunodeficiency (CVID) is the most prevalent antibody impairment. It is characterized by failure in immunoglobulin and protective antibody generation and defined by an increased tendency toward bacterial infections, autoimmunity, and malignancy. Most CVID diagnoses do not follow a classical Mendelian pattern of inheritance. In recent years, CVID has been considered an epigenetic phenomenon in the majority of cases, overtaking previous monogenetic and/or polygenetic theories. The aim of this study was to review the role of microRNAs (miRNAs) in CVID, focusing on the involvement of the same miRNAs in various non-infectious clinical complications of CVID, mainly autoimmunity and/or cancer. Materials and Methods: A bibliographic search of the scientific literature was carried out independently by two researchers in scientific databases and search engines. The MeSH terms “microRNAs” and “common variable immunodeficiency” were used. All research articles from inception to May 2020 were considered. Results: The literature data showed the involvement of two miRNAs in primary immunodeficiency: miR-142 and miR-155. Both of these miRNAs have been investigated through mice models, in which miR-142 and miR-155 were deleted. These knock-out (KO) mice models showed phenotypic analogies to CVID patients with hypogammaglobulinemia, adaptive immunodeficiency, polyclonal proliferation, lung disease, and enteric inflammation. miR-142 and miR-155 have been found to be involved in the following autoimmune and neoplastic clinical complications of CVID: Gastric cancer, gastric mucosa-associated lymphoid tissue (MALT) lymphoma, natural killer/Tcell lymphoma (NKTCL), and immune thrombocytopenia. Conclusions: miR-142 and miR-155 deregulation leads to similar CVID phenotypesin KO mice models. Although no data are available on the involvement of these miRNAs in human CVID, their dysregulation has been detected in human CVID comorbidities. The literature data show that miRNA sequences in murine models are comparable to those in humans; therefore, miR-142 and miR-155 involvement in human CVID could be hypothesized.

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MicroRNAs 142-3p, miR-155 and miR-203 Are Deregulated in Gastric MALT Lymphomas Compared to Chronic Gastritis

Cited by 25 publications

References 43 publications

Helicobacter pylori, gastric cancer and other gastrointestinal malignancies

Helicobacter pylori, gastric cancer and other gastrointestinal malignancies

Helicobacter pylori CagA promotes the malignant transformation of gastric mucosal epithelial cells through the dysregulation of the miR‐155/KLF4 signaling pathway

Involvement of miR-142 and miR-155 in Non-Infectious Complications of CVID

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