Epigenetic modifications induced by RGC-32 in colon cancer

Vlaicu, Sonia I.; Tegla, Cosmin; Cudrici, Cornelia; Fosbrink, Matthew; Nguyen, Vingh; Azimzadeh, Philippe; Rus, Violeta; Chen, Hegang; Mircea, Petru Adrian; Shamsuddin, Abulkalam M.; Rus, Horea

doi:10.1016/j.yexmp.2009.10.010

Cited by 41 publications

(40 citation statements)

References 35 publications

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“…RGC-32 plays a role in the immune response which has been determined [29]. Recent studies reported that levels of RGC-32 mRNA in PBMCs were significantly higher in patients with stable SM as compared with patients who had a relapse (active disease) [8] and the RGC-32 protein expressions in macrophages and T cells were significantly increased in the colonic mucosa of patients with inflammatory bowel disease [9]. Our study demonstrates that not only the plasma RGC-32 levels but intracellular RGC-32 expression of CD4 + T cells were also significantly increased in DCM patients.…”

Section: Discussionmentioning

confidence: 99%

“…In RGC-32-deficient mice, demonstrated that RGC-32 -/-CD4 + T cells exhibited enhanced proliferation, IL-2 production, and Akt phosphorylation as compared with RGC-32 +/+ CD4 + T cells, suggesting a down-regulatory role of RGC-32 under Th0 conditions [7]. Tegla and Vlaicu et al reported increased expression of RGC-32 protein in macrophages, T cells, and astrocytes in the brain of patients with multiple sclerosis (MS) and in the colonic mucosa of patients with inflammatory bowel disease [8,9].…”

Section: Introductionmentioning

confidence: 99%

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Response Gene to Complement-32 Promotes the Imbalance of Treg/Th17 in Patients with Dilated Cardiomyopathy

Li¹,

Zhou²,

Tang³

et al. 2017

Cell Physiol Biochem

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Background/Aims: The imbalance of Treg/Th17 cells plays important role in the pathogenesis of dilated cardiomyopathy (DCM). Response gene to complement (RGC)-32 is a cell cycle regulator that plays an important role in cell proliferation. We evaluated whether the upregulation of RGC-32 was implicated in the homeostasis of Treg/Th17 cells in DCM. Methods:The levels of plasma RGC-32, IL-17 and TGF-β1, and the frequencies of circulating CD4 + RGC-32 + T cells, Th17 and Treg cells in patients with DCM were determined by Cytokinespecific sandwich ELISA and the flow cytometer (FCM), respectively. Results: A significant elevation of plasma RGC-32 in patients with DCM compared with healthy control (HC) subjects was observed. This upregulation was associated with an increase in frequency of Th17 and a decrease in frequency of Treg cells. To further assessed the role of RGC-32, we investigated the effects of RGC-32 up-or down-regulation on frequencies of Th17 and Treg cells in peripheral blood mononuclear cells (PBMCs) from subjects. Importantly, overexpression of RGC-32 was accompanied by an augmentation of Th17 and a reduction of Treg expression. Conclusion: In summary, our study demonstrated the up-regulation of RGC-32 contributed to the imbalance of Treg/Th17 cells in patients with DCM.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Response Gene to Complement-32 Promotes the Imbalance of Treg/Th17 in Patients with Dilated Cardiomyopathy

Li¹,

Zhou²,

Tang³

et al. 2017

Cell Physiol Biochem

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show abstract

“…In human diseases, we have reported increased expression of RGC-32 protein in macrophages, T cells, and astrocytes in the brain of patients with multiple sclerosis (MS) and in the colonic mucosa of patients with inflammatory bowel disease (5, 14). A large body of evidence supports the role of proinflammatory Th17 cells in the pathogenesis of MS and other autoimmune diseases (15–21).…”

mentioning

confidence: 99%

RGC-32 Promotes Th17 Cell Differentiation and Enhances Experimental Autoimmune Encephalomyelitis

Rus

Nguyen

Tatomir

et al. 2017

The Journal of Immunology

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Th17 cells play a critical role in autoimmune diseases, including multiple sclerosis and its animal model, experimental autoimmune encephalomyelitis. Response gene to complement (RGC)-32 is a cell cycle regulator and a downstream target of TGF-β that mediates its profibrotic activity. In this study, we report that RGC-32 is preferentially upregulated during Th17 cell differentiation. RGC-32−/− mice have normal Th1, Th2, and regulatory T cell differentiation but show defective Th17 differentiation in vitro. The impaired Th17 differentiation is associated with defects in IFN regulatory factor 4, B cell–activating transcription factor, retinoic acid–related orphan receptor γt, and SMAD2 activation. In vivo, RGC-32−/− mice display an attenuated experimental autoimmune encephalomyelitis phenotype accompanied by decreased CNS inflammation and reduced frequency of IL-17– and GM-CSF–producing CD4+ T cells. Collectively, our results identify RGC-32 as a novel regulator of Th17 cell differentiation in vitro and in vivo and suggest that RGC-32 is a potential therapeutic target in multiple sclerosis and other Th17-mediated autoimmune diseases.

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“…H2BK15ac Acetylated H2BK15 levels are reported to rise after RGC-32 knockdown in colon cancer cell lines (86).…”

Section: H2bk5acmentioning

confidence: 99%

Study of the Epigenetic Signals in the Human Genome

Ferreira

Afreixo

Moura

et al. 2017

11th International Conference on Practical Applications of Computational Biology &Amp; Bioinformatics

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Epigenetic modifications induced by RGC-32 in colon cancer

Cited by 41 publications

References 35 publications

Response Gene to Complement-32 Promotes the Imbalance of Treg/Th17 in Patients with Dilated Cardiomyopathy

Response Gene to Complement-32 Promotes the Imbalance of Treg/Th17 in Patients with Dilated Cardiomyopathy

RGC-32 Promotes Th17 Cell Differentiation and Enhances Experimental Autoimmune Encephalomyelitis

Study of the Epigenetic Signals in the Human Genome

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