Reduced Histone H3 Lysine 9 Methylation Contributes to the Pathogenesis of Latent Autoimmune Diabetes in Adults via Regulation of SUV39H2 and KDM4C

Liu, Xiyu; Li, Hong

doi:10.1155/2017/8365762

Cited by 3 publications

(3 citation statements)

References 26 publications

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“… 85,101 Dysregulation of SUV39H2 has also been reported in several other diseases, such as hereditary nasal parakeratosis, which is caused by a mutation of SUV39H2 in dogs. 102 Moreover, it has been reported that alterations in the regulation of SUV39H2 are also associated with autoimmune diabetes 103 and steatohepatitis in mice. 104 …”

Section: Introductionmentioning

confidence: 99%

Lysine methyltransferase inhibitors: where we are now

et al. 2022

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Section: Introductionmentioning

confidence: 99%

Lysine methyltransferase inhibitors: where we are now

et al. 2022

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“…A mutation of SUV39H2 was reported to be responsible for hereditary nasal parakeratosis [ 19 ]; this provided us insights into SUV39H2-mediated epigenetic regulation in keratinocytes. Additionally, dysregulation of SUV39H2 mediated by H3K9me3 is associated with autoimmune diabetes [ 20 ] and steatohepatitis [ 21 ] in mice. The activity of SUV39H2 is modulated in various manners.…”

Section: Introductionmentioning

confidence: 99%

Identification of SUV39H2 as a potential oncogene in lung adenocarcinoma

Zheng

Wang

et al. 2018

Clin Epigenet

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BackgroundSUV39H2 (suppressor of variegation 3-9 homolog 2), which introduces H3K9me3 to induce transcriptional repression, has been reported to play critical roles in heterochromatin maintenance, DNA repair, and recently, carcinogenesis. Dysregulation of SUV39H2 expression has been observed in several types of cancers. However, neither the genomic landscape nor the clinical significance of SUV39H2 in lung adenocarcinoma has been probed comprehensively.MethodsIn this research, we conducted bioinformatics analysis to primarily sort out potential genes with dysregulated expressions. After we identified SUV39H2, RNA-seq was performed for a high-throughput evaluation of altered gene expression and dysregulated pathways, followed by a series of validations via RT-qPCR and bioinformatics analyses. Finally, to assess the potential oncogenic role of SUV39H2, we employed the invasion assay and clone formation assay in vitro and tumorigenesis assays in mouse models in vivo.ResultsThrough bioinformatics analyses, we found that SUV39H2 underwent a severe upregulation in the tumor tissue, which was also confirmed in the surgically removed tissues. Overexpression of SUV39H2 was mainly associated with its amplification and with shorter patient overall survival. Then, the RNA-seq demonstrated that TPM4, STOM, and OPTN might be affected by the loss of function of SUV39H2. Finally, in vitro and in vivo experiments with SUV39H2 knockdown all suggested a potential role of SUV39H2 in both carcinogenesis and metastasis.ConclusionsSUV39H2 expression was elevated in lung adenocarcinoma. TPM4, OPTN, and STOM were potentially regulated by SUV39H2. SUV39H2 might be a potential oncogene in lung adenocarcinoma, mediating tumorigenesis and metastasis.Electronic supplementary materialThe online version of this article (10.1186/s13148-018-0562-4) contains supplementary material, which is available to authorized users.

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“…SUV39H2 downregulation has been also associated with autoimmune diseases. Decreased expression levels of SUV39H2 and reduction of global H3 lysine 9 methylation has been evidenced in CD4+ T cells from Latent autoimmune diabetes patients [ 73 ]. These data correlate with the miRNAs pattern of CD patients found in this study (Fig.…”

Section: Discussionmentioning

confidence: 99%

MicroRNAs overexpressed in Crohn’s disease and their interactions with mechanisms of epigenetic regulation explain novel aspects of Crohn’s disease pathogenesis

et al. 2021

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Background In this review, we were interested to identify the wide universe of enzymes associated with epigenetic modifications, whose gene expression is regulated by miRNAs with a high relative abundance in Crohn's disease (CD) affected tissues, with the aim to determine their impact in the pathogenesis and evolution of the disease. Methods We used HMDD and Bibliometrix R-package in order to identify the miRNAs overexpressed in CD. The identified enzymes associated with epigenetic mechanisms and post-translational modifications, regulated by miRNAs upregulated in CD, were analyzed using String v11 database. Results We found 190 miRNAs with great abundance in patients with CD, of which 26 miRNAs regulate the gene expression of enzymes known to catalyze epigenetic modifications involved in essentials pathophysiological processes, such as chromatin architecture reorganization, immune response regulation including CD4+ T cells polarization, integrity of gut mucosa, gut microbiota composition and tumorigenesis. Conclusion The integrated analysis of miRNAs with a high relative abundance in patients with CD showed a combined and superimposed gene expression regulation of enzymes associated with relevant epigenetic mechanisms and that could explain, in part, the pathogenesis of CD.

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Reduced Histone H3 Lysine 9 Methylation Contributes to the Pathogenesis of Latent Autoimmune Diabetes in Adults via Regulation of SUV39H2 and KDM4C

Cited by 3 publications

References 26 publications

Lysine methyltransferase inhibitors: where we are now

Lysine methyltransferase inhibitors: where we are now

Identification of SUV39H2 as a potential oncogene in lung adenocarcinoma

MicroRNAs overexpressed in Crohn’s disease and their interactions with mechanisms of epigenetic regulation explain novel aspects of Crohn’s disease pathogenesis

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