title: Overexpression of miR-142-5p and miR-155 in gastric mucosa-associated lymphoid tissue (MALT) lymphoma resistant to Helicobacter pylori eradication.
abstract: microRNAs (miRNAs) are small non-coding RNAs that can function as endogenous silencers of target genes and play critical roles in human malignancies. To investigate the molecular pathogenesis of gastric mucosa-associated lymphoid tissue (MALT) lymphoma, the miRNA expression profile was analyzed. miRNA microarray analysis with tissue specimens from gastric MALT lymphomas and surrounding non-tumor mucosae revealed that a hematopoietic-specific miRNA miR-142 and an oncogenic miRNA miR-155 were overexpressed in MALT lymphoma lesions. The expression levels of miR-142-5p and miR-155 were significantly increased in MALT lymphomas which do not respond to Helicobacter pylori (H. pylori) eradication. The expression levels of miR-142-5p and miR-155 were associated with the clinical courses of gastric MALT lymphoma cases. Overexpression of miR-142-5p and miR-155 was also observed in Helicobacter heilmannii-infected C57BL/6 mice, an animal model of gastric MALT lymphoma. In addition, miR-142-5p and miR-155 suppress the proapoptotic gene TP53INP1 as their target. The results of this study indicate that overexpression of miR-142-5p and miR-155 plays a critical role in the pathogenesis of gastric MALT lymphoma. These miRNAs might have potential application as therapeutic targets and novel biomarkers for gastric MALT lymphoma.
authors.affiliation: Division of Gastroenterology and Hepatology, Department of Internal Medicine, Shinjuku-ku, Tokyo, Japan.
authors.forename: Yoshimasa
authors.initials: Y
authors.lastname: Saito
authors.forename: Hidekazu
authors.initials: H
authors.lastname: Suzuki
authors.forename: Hitoshi
authors.initials: H
authors.lastname: Tsugawa
authors.forename: Hiroyuki
authors.initials: H
authors.lastname: Imaeda
authors.forename: Juntaro
authors.initials: J
authors.lastname: Matsuzaki
authors.forename: Kenro
authors.initials: K
authors.lastname: Hirata
authors.forename: Naoki
authors.initials: N
authors.lastname: Hosoe
authors.forename: Masahiko
authors.initials: M
authors.lastname: Nakamura
authors.forename: Makio
authors.initials: M
authors.lastname: Mukai
authors.forename: Hidetsugu
authors.initials: H
authors.lastname: Saito
authors.forename: Toshifumi
authors.initials: T
authors.lastname: Hibi
mesh_terms: D000328:Adult; D000368:Aged; D000818:Animals; D000900:Anti-Bacterial Agents / Q000494:pharmacology / Q000627:therapeutic use; D001483:Base Sequence; D014408:Biomarkers, Tumor; D002097:C-Reactive Protein / Q000235:genetics; D004195:Disease Models, Animal; D005260:Female; D005753:Gastric Mucosa / Q000378:metabolism / Q000382:microbiology / Q000473:pathology; D015870:Gene Expression; D015972:Gene Expression Regulation, Neoplastic; D016481:Helicobacter Infections / Q000188:drug therapy; D018247:Helicobacter heilmannii / Q000187:drug effects; D006801:Humans; D018442:Lymphoma, B-Cell, Marginal Zone / Q000235:genetics*; D008297:Male; D051379:Mice; D035683:MicroRNAs / Q000737:chemistry / Q000235:genetics*; D008875:Middle Aged; D008969:Molecular Sequence Data; D009419:Nerve Tissue Proteins / Q000235:genetics; D015514:Oncogene Proteins, Fusion / Q000235:genetics; D013274:Stomach Neoplasms / Q000235:genetics*; D014178:Translocation, Genetic; D016159:Tumor Suppressor Protein p53 / Q000235:genetics; D000099153:Pentraxins
chemical_list: D000900:Anti-Bacterial Agents; D014408:Biomarkers, Tumor; D002097:C-Reactive Protein; D035683:MicroRNAs; D009419:Nerve Tissue Proteins; D015514:Oncogene Proteins, Fusion; D016159:Tumor Suppressor Protein p53; D000099153:Pentraxins; C415943:API2-MALT1 fusion protein, human; C555159:MIRN142 microRNA, human; C524942:MIRN155 microRNA, human