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Review
. 2016 Dec;73(24):4599-4610.
doi: 10.1007/s00018-016-2308-9. Epub 2016 Jul 27.

Epigenetic roles in the malignant transformation of gastric mucosal cells

Jun Tie  1 , Xiangyuan Zhang  1 , Daiming Fan  2
Affiliations
Review

Epigenetic roles in the malignant transformation of gastric mucosal cells

Jun Tie et al. Cell Mol Life Sci. 2016 Dec.

Abstract

Gastric carcinogenesis occurs when gastric epithelial cells transition through the initial, immortal, premalignant, and malignant stages of transformation. Epigenetic regulations contribute to this multistep process. Due to the critical role of epigenetic modifications , these changes are highly likely to be of clinical use in the future as new biomarkers and therapeutic targets for the early detection and treatment of cancers. Here, we summarize the recent findings on how epigenetic modifications, including DNA methylation, histone modifications, and non-coding RNAs, regulate gastric carcinogenesis, and we discuss potential new strategies for the diagnosis and treatments of gastric cancer. The strategies may be helpful in the further understanding of epigenetic regulation in human diseases.

Keywords: Epigenetic roles; Gastric mucosal cells; Helicobacter pylori; Malignant transformation.

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Figures

Fig. 1
Fig. 1
NcRNA-oriented network in the malignant transformation process of gastric cancer. This figure provides insight into the roles of ncRNA and its related protein in the malignant transformation of gastric mucosal cells. It can be seen that a complex network composed of ncRNA and its upstream and downstream components affects the malignant transformation of gastric mucosal cells
Fig. 2
Fig. 2
Epigenetic regulation of RUNX3 in the malignant transformation of gastric mucosal cells. MiR-146a/b and miR-148 directly inhibited UHRF1 and DNMT3b, respectively. Downregulation of miR-146a/b and miR-148 led to the increase in UHRF1 and DNMT3b, and this effect in turn inactivated RUNX3 via promoter methylation in gastric cancer. In addition, increased H3K9 dimethylation and reduced H3 acetylation, as well as the increased miR-130b, miR-301a, miR-106a, miR-103a, miR-495, and miR-532-5p, synergistically inhibited the expression of RUNX3
See this image and copyright information in PMC

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