HMGB1 Recruits TET2/AID/TDG to Induce DNA Demethylation in STAT3 Promoter in CD4<sup>+</sup> T Cells from aGVHD Patients

Xu, Xuejun; Chen, Yan; Liu, Enyi; Fu, Bin; Hua, Juan; Chen, Xu; Xu, Yajing

doi:10.1155/2020/7165230

Cited by 3 publications

(2 citation statements)

References 45 publications

(51 reference statements)

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“…Intriguingly, Xu et al demonstrated that HMGB1 can enhance the methylation of STAT3 promoter by recruiting TET2/AID/TDG to the STAT3 promoter region, resulting in the high expression of STAT3 in CD4 + T cells, suggesting that HMGB1 may be involved in epigenetic regulation 83 .…”

Section: The Biology Of Hmgb1mentioning

confidence: 99%

Targeting HMGB1: An available Therapeutic Strategy for Breast Cancer Therapy

2022

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HMGB1 is a member of highly conserved high mobility group protein superfamily with intracellular and extracellular distribution. Abnormal HMGB1 levels are frequently manifested in various malignant diseases, including breast cancer. Numerous studies have revealed the clinical value of HMGB1 in the diagnosis and therapy of breast cancer. However, the dual function of pro- and anti-tumor makes HMGB1 in cancer progression requires more profound understanding. This review summarizes the functions and mechanisms of HMGB1 on regulating breast cancer, including autophagy, immunogenic cell death, and interaction with the tumor microenvironment. These functions determine the strategies for the development of chemotherapy, radiotherapy, immunotherapy and combination therapies by targeting HMGB1 in breast cancer. Defining the mechanisms of HMGB1 on regulating breast cancer development and progression will facilitate the application of HMGB1 as a therapeutic target for breast cancer.

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Section: The Biology Of Hmgb1mentioning

confidence: 99%

Targeting HMGB1: An available Therapeutic Strategy for Breast Cancer Therapy

2022

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“…The protein extract was centrifuged at 13,200 rpm and the supernatant was collected, and incubated with 50 μL magnetic beads on ice. Next, HGMB1 or STAT3 antibody was added to the supernatant, incubated overnight at 4 °C, and tested by Western blot [31,32].…”

Section: Co-immunoprecipitation (Co-ip) Assaymentioning

confidence: 99%

microRNA-193-3p attenuates myocardial injury of mice with sepsis via STAT3/HMGB1 axis

et al. 2021

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Objective Little is known regarding the functional role of microRNA-193-3p (miR-193-3p) in sepsis. Hence, the aim of the present study was to investigate the effect of miR-193-3p on myocardial injury in mice with sepsis and its mechanism through the regulation of signal transducers and activators of transcription 3 (STAT3). Methods The mice model of sepsis was established by cecal ligation and puncture (CLP), septic mice were injected with miR-193-3p agomir, miR-193-3p antagomir or siRNA-STAT3. The expression of miR-193-3p, STAT3 and HMGB1 in the myocardial tissue of septic mice were detected. Cardiac ultrasound, hemodynamics, myocardial injury markers, inflammatory factors and cardiomyocyte apoptosis in septic mice were measured. Results MiR-193-3p expression was reduced while STAT3 expression was increased in septic mice. Down-regulated STAT3 or up-regulated miR-193-3p improved cardiac function, attenuated myocardial injury, inflammation and cardiomyocyte apoptosis in septic mice. Knockdown STAT3 reversed the role of inhibited miR-193-3p for mice with sepsis. miR-193-3p targeted STAT3, thereby inhibiting HMGB1 expression. Conclusion This study provides evidence that miR-193-3p targets STAT3 expression to reduce HMGB1 expression, thereby reducing septic myocardial damage. MiR-193-3p might be a potential candidate marker and therapeutic target for sepsis.

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CMV infection combined with acute GVHD associated with poor CD8+ T-cell immune reconstitution and poor prognosis post-HLA-matched allo-HSCT

Fan

Han

Zuo

et al. 2022

Clinical and Experimental Immunology

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Cytomegalovirus (CMV) infection and acute graft-versus-host disease (aGVHD) are two major complications that contribute to a poor prognosis after hematopoietic stem cell transplantation (HSCT). Superior early immune reconstitution (IR) is associated with improved survival after HSCT. However, when all three factors, CMV infection, aGVHD, and IR, are concomitantly considered, the effects of the triple events on HSCT are still unknown and should be studied further. Thus we enrolled 185 patients who were diagnosed as hematological malignancies and treated with HLA-matched sibling transplantation (MST) between January 2010 and December 2014, of whom 83 were positive for CMV infection and 82 had aGVHD. Results showed that patients with both aGVHD and CMV infection had significantly higher non-relapse mortality (NRM), lower overall survival (OS), and delayed CD8+ T-cell IR. Multivariate analyses showed that both aGVHD combined with CMV infection and delayed CD8+ T-cell IR were independent risk factors for post-MST prognosis. Recurrent CMV infections are associated with poor CD8+ T-cell reconstitution. However, superior IR could protect against the negative effects of aGVHD and CMV infection on the transplant outcomes.

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HMGB1 Recruits TET2/AID/TDG to Induce DNA Demethylation in STAT3 Promoter in CD4⁺ T Cells from aGVHD Patients

Cited by 3 publications

References 45 publications

Targeting HMGB1: An available Therapeutic Strategy for Breast Cancer Therapy

Targeting HMGB1: An available Therapeutic Strategy for Breast Cancer Therapy

microRNA-193-3p attenuates myocardial injury of mice with sepsis via STAT3/HMGB1 axis

CMV infection combined with acute GVHD associated with poor CD8+ T-cell immune reconstitution and poor prognosis post-HLA-matched allo-HSCT

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HMGB1 Recruits TET2/AID/TDG to Induce DNA Demethylation in STAT3 Promoter in CD4+ T Cells from aGVHD Patients

Cited by 3 publications

References 45 publications

Targeting HMGB1: An available Therapeutic Strategy for Breast Cancer Therapy

Targeting HMGB1: An available Therapeutic Strategy for Breast Cancer Therapy

microRNA-193-3p attenuates myocardial injury of mice with sepsis via STAT3/HMGB1 axis

CMV infection combined with acute GVHD associated with poor CD8+ T-cell immune reconstitution and poor prognosis post-HLA-matched allo-HSCT

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HMGB1 Recruits TET2/AID/TDG to Induce DNA Demethylation in STAT3 Promoter in CD4⁺ T Cells from aGVHD Patients