ArticleCell communication and signaling : CCS2019
Inhibition of Bcl6b promotes gastric cancer by amplifying inflammation in mice.
Article in Cell communication and signaling : CCS, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 17 citations in OpenAlex.
- BCL6B suppresses acute myeloid leukemia progression by transcriptionally repressing GGT5 and modulating MAPK signaling.Biology direct · 2026Article
- Insight into the Role of the BCL6B Gene in Biological Functions and Disease Progression.Journal of Cancer · 2025Review
- USP29 activation mediated by FUBP1 promotes AURKB stability and oncogenic functions in gastric cancer.Cancer cell international · 2024Article
- Dynamic changes of DNA methylation induced by benzo(a)pyrene in cancer.Genes and environment : the official journal of the Japanese Environmental Mutagen Society · 2023Review
- Prevention of malignant digestive system tumors should focus on the control of chronic inflammation.World journal of gastrointestinal oncology · 2023Review
- Transcription of the Envelope Protein by 1-L Protein-RNA Recognition Code Leads to Genes/Proteins That Are Relevant to the SARS-CoV-2 Life Cycle and Pathogenesis.Current issues in molecular biology · 2022Article
- Identification of New Genes Involved in Germline Predisposition to Early-Onset Gastric Cancer.International journal of molecular sciences · 2021Article
- Hormone-Related Cancer and Autoimmune Diseases: A Complex Interplay to be Discovered.Frontiers in genetics · 2021Review
- High expression of TREM2 promotes EMT via the PI3K/AKT pathway in gastric cancer: bioinformatics analysis and experimental verification.Journal of Cancer · 2021Article
Corrections and comments
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundChronic gastritis has been demonstrated to be a key cause of gastric cancer (GC), and control of gastric inflammation is regarded as an effective treatment for the clinical prevention of gastric carcinogenesis. However, there remains an unmet need to identify the dominant regulators of gastric oncogenesis-associated inflammation in vivo.
methodsThe mouse model for the study of inflammation-associated GC was induced by Benzo[a]pyrene (BaP) intragastric administration in Bcl6b
resultsBcl6b was gradually downregulated by its own promoter hypermethylation in parallel to an increasing inflammatory response during the progression of BaP-induced gastric carcinogenesis in mice. Moreover, knockout of Bcl6b dramatically worsened the severity of gastric cancer and aggravated the inflammatory response in the BaP-induced mice GC model. Re-activation of Bcl6b by 5-Aza impeded inflammatory amplification and BaP-induced GC development, prolonging survival time in wildtype mice, whereas no notable curative effect occurred in Bcl6b
conclusionsEpigenetic inactivation of Bcl6b promotes gastric cancer through amplification of the gastric inflammatory response in vivo and offers a new approach for GC treatment and regenerative medicine.
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