ArticleDigestive diseases and sciences2017
SOX2 Inhibition Promotes Promoter Demethylation of CDX2 to Facilitate Gastric Intestinal Metaplasia.
Article in Digestive diseases and sciences, 2017. 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.
- Weiyan Tongluo Granules attenuate gastric intestinal metaplasia through PPARγ/NF-κB/CDX2 signaling pathway.Chinese medicine · 2026Article
- Exploration of gastric carcinogenesis from the relationship between bile acids and intestinal metaplasia and intragastric microorganisms (H. pylori and non-H. pylori).Journal of cancer research and clinical oncology · 2023Review
- The role of bile acid in intestinal metaplasia.Frontiers in physiology · 2023Review
- 5-azacytidine inhibits Sox2 promoter methylation during the induction of Thy-1American journal of translational research · 2023Article
- CDX2-induced intestinal metaplasia in human gastric organoids derived from induced pluripotent stem cells.iScience · 2022Article
- Roles and action mechanisms of bile acid-induced gastric intestinal metaplasia: a review.Cell death discovery · 2022Review
- Derivation of Mouse Parthenogenetic Advanced Stem Cells.International journal of molecular sciences · 2021Article
- Digital image analysis of multiplex fluorescence IHC in colorectal cancer recognizes the prognostic value of CDX2 and its negative correlation with SOX2.Laboratory investigation; a journal of technical methods and pathology · 2020Article
- SOX2 interferes with the function of CDX2 in bile acid-induced gastric intestinal metaplasia.Cancer cell international · 2019Article
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Authors and funding
4 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundGastric intestinal metaplasia (IM) is regarded as a premalignant lesion, conferring risks for gastric cancer development. An intestinal transcription factor, CDX2, plays a vital role in establishing and maintaining IM. SOX2, an HMG-box transcription factor, is expressed in normal gastric mucosa and downregulated in IM. Therefore, it is important to elucidate the mutual interaction of SOX2 and CDX2 in gastric IM.
aimsThis study aims to evaluate the negative correlation between SOX2 and CDX2 in mRNA expression and promoter methylation and to illuminate the effect of SOX2 on the promoter methylation of CDX2.
methodsImmunohistochemistry, real-time PCR and methylation-specific polymerase chain reaction assays were performed to evaluate the expression and promoter methylation of SOX2 and CDX2 in IM tissues from patients. SOX2 knockdown and CDX2 overexpression were performed in GES-1 cells to further clarify the relationship between SOX2 and CDX2.
resultsA negative correlation between SOX2 and CDX2 was found in 120 gastric IM specimens. Additionally, significant DNA demethylation of CDX2 promoter in clinical IM specimens was observed concomitantly with partial methylation of the SOX2 promoter. Furthermore, SOX2 knockdown in GES-1 cells triggered promoter demethylation of CDX2. Finally, the phenotype shift of gastric intestinal metaplasia in GES-1 cells, marked by MUC2 expression, was effectively induced by the combination of SOX2 RNAi and CDX2 overexpression.
conclusionsAberrant DNA methylation of SOX2 and CDX2 genes contributes to the development of IM. Notably, SOX2 may play a role in establishing and maintaining the methylation status of the CDX2 gene in gastric tissues and cells.
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