Dataset Information

Downregulation of miR‑7 and miR‑153 is involved in Helicobacter pylori CagA induced gastric carcinogenesis and progression.

ABSTRACT: Helicobacter pylori (H. pylori) infection plays a pivotal role in the development of gastric cancer (GC). However, the association between aberrant microRNAs (miRNAs/miRs) expression and H. pylori‑induced GC remains poorly understood. The present study reported that repeated infection of H. pylori caused the oncogenicity of GES‑1 cells in BALB/c Nude mice. miRNA sequencing revealed that both miR‑7 and miR‑153 were significantly decreased in the cytotoxin‑associated gene A (CagA) positive GC tissues and this was further confirmed in a chronic infection model of GES‑1/HP cells. Further biological function experiments and in vivo experiments validated that miR‑7 and miR‑153 can promote apoptosis and autophagy, inhibit proliferation and inflammatory response in GES‑1/HP cells. All the associations between miR‑7/miR‑153 and their potential targets were revealed via bioinformatics prediction and dual‑luciferase reporter assay. Particularly, downregulation of both miR‑7 and miR‑153 obtained an improved sensitivity and specificity in diagnosing H. pylori (CagA+)‑induced GC. The present study identified that the combination of miR‑7 and miR‑153 may be regarded as novel therapeutic targets in H. pylori CagA (+)‑associated GC.

SUBMITTER: Song Y

PROVIDER: S-EPMC10237257 | biostudies-literature | 2023 Jul

REPOSITORIES: biostudies-literature

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Downregulation of miR‑7 and miR‑153 is involved in Helicobacter pylori CagA induced gastric carcinogenesis and progression.

Song Yu Y Guo Dong D Liu Jia-Fei JF Ge Li-Na LN Liu Peng P Qu Ye-Min YM Cong Hai-Yan HY Li Tian T Chang Xin X Wang Yi-Ran YR Shao Li-Ying LY Du Zong-Jun ZJ Wang Ming-Yi MY

International journal of oncology 20230526 1

Helicobacter pylori (H. pylori) infection plays a pivotal role in the development of gastric cancer (GC). However, the association between aberrant microRNAs (miRNAs/miRs) expression and H. pylori‑induced GC remains poorly understood. The present study reported that repeated infection of H. pylori caused the oncogenicity of GES‑1 cells in BALB/c Nude mice. miRNA sequencing revealed that both miR‑7 and miR‑153 were significantly decreased in the cytotoxin‑associated ge ...[more]

PMID: 37232358

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Project description:To clarify the mechanisms of connexin 32 (Cx32) downregulation by potential transcriptional factors (TFs) in Helicobacter pylori (H. pylori)-associated gastric carcinogenesis.Approximately 25 specimens at each developmental stage of gastric carcinogenesis [non-atrophic gastritis, chronic atrophic gastritis, intestinal metaplasia, dysplasia and gastric carcinoma (GC)] with H. pylori infection [H. pylori (+)] and 25 normal gastric mucosa (NGM) without H. pylori infection [H. pylori (-)] were collected. After transcriptional factor array analysis, the Cx32 and PBX1 expression levels of H. pylori-infected tissues from the developmental stages of GC and NGM with no H. pylori infection were measured by real-time polymerase chain reaction (RT-PCR) and Western blot analysis. Regarding H. pylori-infected animal models, the Cx32 and PBX1 mRNA expression levels and correlation between the gastric mucosa from 10 Mongolian gerbils with long-term H. pylori colonization and 10 controls were analyzed. PBX1 and Cx32 mRNA and protein levels were further studied under the H. pylori-infected condition as well as PBX1 overexpression and knockdown conditions in vitro.Incremental PBX1 was first detected by TF microarray in H. pylori-related gastric carcinogenesis. The identical trend of PBX1 and Cx32 expression was confirmed in the developmental stages of H. pylori-related clinical specimens. The negative correlation of PBX1 and Cx32 was confirmed in H. pylori-infected Mongolian gerbils. Furthermore, decreased PBX1 expression was detected in the normal gastric epithelial cell line GES-1 with H. pylori infection. Enforced overexpression or RNAi-mediated knockdown of PBX1 contributed to the diminished or restored Cx32 expression in GES-1 and the gastric carcinoma cell line BGC823, respectively. Finally, dual-luciferase reporter assay in HEK293T cells showed that Cx32 promoter activity decreased by 30% after PBX1 vector co-transfection, indicating PBX1 as a transcriptional downregulator of Cx32 by directly binding to its promoters.PBX1 is one of the determinants in the Cx32 promoter targeting site, preventing further damage of gap junction protein in H. pylori-associated gastric carcinogenesis.

Dataset Information

Downregulation of miR‑7 and miR‑153 is involved in Helicobacter pylori CagA induced gastric carcinogenesis and progression.

Publications

Downregulation of miR‑7 and miR‑153 is involved in <i>Helicobacter pylori</i> CagA induced gastric carcinogenesis and progression.

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