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Deregulation of miRNA in -Induced Gastric MALT Lymphoma: From Mice to Human. | LitMetric

Deregulation of miRNA in -Induced Gastric MALT Lymphoma: From Mice to Human.

J Clin Med

INSERM, Université Bordeaux, UMR1053 Bordeaux Research in Translational Oncology, BaRITOn, 33000 Bordeaux, France.

Published: June 2019

AI Article Synopsis

  • MicroRNAs (miRNAs) are tiny non-coding RNA molecules that can influence inflammation and cancer development, and previous studies suggested that five specific miRNAs may be important in GML progression in mice.
  • In this study comparing GML mouse model findings to actual human cases, researchers found four miRNAs were increased and two were decreased in GML patients, suggesting these miRNAs may work together to promote the development of GML.

Article Abstract

Gastric MALT lymphoma (GML) is directly caused by infection but occurs only in a small number of infected subjects. Mechanisms underlying the initiation and progression of GML remain unclear. MicroRNAs (miRNAs) are small non-coding RNAs that are now considered as major players in inflammation and carcinogenesis, acting as oncogenes or tumor suppressors. Previous laboratory studies have shown in a GML mouse model that overexpression of a distinct set of five miRNAs (miR-21a, miR-135b, miR-142a, miR-150, miR-155) could play a critical role in the pathogenesis of GML. Our goal was to compare the miRNA expression profile obtained in the GML mouse model to that in human GML (11 cases of GML compared to 17 cases of gastritis control population). RTqPCR on the five dysregulated miRNAs in the GML mouse model and PCR array followed by RTqPCR confirmation showed that four miRNAs were up-regulated (miR-150, miR-155, miR-196a, miR-138) and two miRNAs down-regulated (miR-153, miR-7) in the stomachs of GML patients vs. gastritis control population. The analysis of their validated targets allowed us to postulate that these miRNAs (except miR-138) could act synergistically in a common signaling cascade promoting lymphomagenesis and could be involved in the pathogenesis of GML.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6616415PMC
http://dx.doi.org/10.3390/jcm8060845DOI Listing

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