Mutual interaction between BCL6 and microRNAs in T cell differentiation

Wei, Zhiyuan; Gao, Weiying; Wu, Yuzhang; Ni, Bing; Tian, Yi

doi:10.1080/15476286.2015.1017232

Cited by 8 publications

(5 citation statements)

References 79 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…More importantly, several studies have uncovered the interaction of BCL-6 with multiple miRNAs in T cell differentiation and malignancies. 25,26 Expanding on this, in the context of OGD-treated cardiomyocytes, we identified re-expressed BCL-6 serves as an upstream regulator of miR-34a expression by recruiting EZH2 to the promoter region of miR-34a through the mediation of H3K27me3 levels. Coincidentally, as a histone methyltransferase, EZH2 possesses the ability to catalyze H3K27me3 in correlation with gene silencing and chromatin compaction; for instance, EZH2 regulates H3K27me3 to downregulate the expression of cyclin dependent kinase 2A.…”

Section: Discussionmentioning

confidence: 79%

BCL‐6 promotes the methylation of miR‐34a by recruiting EZH2 and upregulating CTRP9 to protect ischemic myocardial injury

et al. 2021

View full text Add to dashboard Cite

Acute myocardial infarction (AMI) and the following heart failure are public health problems faced all over the globe. The current study set out to investigate the role of B-cell lymphoma 6 (BCL-6) in cardiac protection after AMI.Initially, AMI mouse models and H9c2 cell oxygen-glucose deprivation (OGD) models were established. The cell models were transfected with the vectors containing oe-BCL-6, oe-EZH2, sh-EZH2, miR-34a mimic, and miR-34a inhibitor. RT-qPCR and Western blot analysis were applied to detect the expression patterns of microRNA-34a (miR-34a), BCL-6, enhancer of zeste homolog 2 (EZH2), and C1q tumor necrosis factor-related protein 9 (CTRP9) in the treated cell models. ChIP-qPCR and co-immunoprecipitation assay were performed to detect EZH2 enrichment and H3K27me3 levels in the miR-34a promoter region and the interaction between BCL-2 and EZH2, respectively. EdU staining, TUNEL staining, and flow cytometry were performed to detect cell proliferation and apoptosis, while ELISA was conducted to detect the oxidative stress levels. It was found that miR-34a was highly expressed in heart tissues of AMI models, while BCL-6 and EZH2 were poorly expressed. BCL-2 overexpression increased the recruitment of EZH2, upregulated H3K27me3 level in the miR-34a promoter region, and inhibited the miR-34a expression. Ctrp9, the downstream negative-regulatory molecule of miR-34a, was upregulated. Besides, miR-34a/CTRP9 expression changes were found to affect cardiomyocyte apoptosis, oxidation stress, and proliferation, and prevent myocardial injury in AMI mice. Our findings indicate that BCL-6 increases the level of H3K27me3 in the promoter region of miR-34a via EZH2 recruitment and CTRP9 upregulation, which inhibits the apoptosis of myocardial cells.

show abstract

Section: Discussionmentioning

confidence: 79%

BCL‐6 promotes the methylation of miR‐34a by recruiting EZH2 and upregulating CTRP9 to protect ischemic myocardial injury

et al. 2021

View full text Add to dashboard Cite

show abstract

“…Ectopic miR-21 overexpression polarizes T-cell differentiation into the Th2 cell subset through increasing GATA3 expression in vitro [82,83]. Furthermore, previous experiments provided a large body of evidence to define miR-21 as a major target for BCL-6, which is downregulated through binding of BCL6 to the corresponding promoter [84]. A molecular study indicated the role of miR-21 in the promotion of the Th2 cell response through repressing IL-12 secretion [44,85].…”

Section: Th2 Cellsmentioning

confidence: 99%

Crosstalk of Transcriptional Regulators of Adaptive Immune System and microRNAs: An Insight into Differentiation and Development

Boshtam

Rahimmanesh

Shariati

et al. 2023

Cells

View full text Add to dashboard Cite

MicroRNAs (miRNAs), as small regulatory RNA molecules, are involved in gene expression at the post-transcriptional level. Hence, miRNAs contribute to gene regulation of various steps of different cell subsets’ differentiation, maturation, and activation. The adaptive immune system arm, which exhibits the most specific immune responses, is also modulated by miRNAs. The generation and maturation of various T-cell subsets concomitant with B-cells is under precise regulation of miRNAs which function directly on the hallmark genes of each cell subset or indirectly through regulation of signaling pathway mediators and/or transcription factors involved in this maturation journey. In this review, we first discussed the origination process of common lymphocyte progenitors from hematopoietic stem cells, which further differentiate into various T-cell subsets under strict regulation of miRNAs and transcription factors. Subsequently, the differentiation of B-cells from common lymphocyte progenitors in bone marrow and periphery were discussed in association with a network of miRNAs and transcription factors.

show abstract

“…HBX can also induce aberrant expression of microRNAs (miRNAs), and this infection-related process has been shown to contribute to the pathogenesis of HCC (Esteller, 2011;Xu et al, 2013;Wu et al, 2014). miRNAs can function on either oncogenes or tumor suppressor genes to mediate tumorigenesis (Wei et al, 2015). The presence of HBX has been shown to be significantly associated with alterations in the host miRNA profile (Trang et al, 2008).…”

Section: Introductionmentioning

confidence: 99%

Contribution of hepatitis B virus X protein-induced aberrant microRNA expression to hepatocellular carcinoma pathogenesis

Wei¹,

Shen²,

Ni³

et al. 2019

Turk J Biol

Self Cite

View full text Add to dashboard Cite

The hepatitis B virus-encoded X (HBX) protein plays important roles in Hepatocellular carcinoma (HCC). Previous studies have demonstrated that HBX can induce alterations in the expression of numerous microRNAs (miRNAs) involved in the carcinogenesis of various tumors. However, the global profile of liver miRNA changes induced by HBX has not been characterized. In this study, we conducted a miRNA microarray analysis to investigate the influence of HBX on the expression of total miRNAs in liver in relation to HCC. Comparative analysis of the data from human normal liver cells (L02) and human HCC cells (HepG2), with or without HBX, identified 19 differentially expressed miRNAs, including 5 with known association to HBX. Target gene prediction for the aberrantly expressed miRNAs identified a total of 304 potential target genes, involved in sundry pathways. Finally, pathway analysis of the HBXinduced miRNAs pathway showed that 5 of the total miRNAs formed an internetwork, suggesting that HBX might exert its pathological effects on hepatic cells through functional synergy with miRNAs that regulated common pathways in liver cells. Therefore, this work provides new insights into the mechanisms of HCC as well as potential diagnostic markers or therapeutic targets for use in clinical management of HCC.

show abstract

Mutual interaction between BCL6 and microRNAs in T cell differentiation

Cited by 8 publications

References 79 publications

BCL‐6 promotes the methylation of miR‐34a by recruiting EZH2 and upregulating CTRP9 to protect ischemic myocardial injury

BCL‐6 promotes the methylation of miR‐34a by recruiting EZH2 and upregulating CTRP9 to protect ischemic myocardial injury

Crosstalk of Transcriptional Regulators of Adaptive Immune System and microRNAs: An Insight into Differentiation and Development

Contribution of hepatitis B virus X protein-induced aberrant microRNA expression to hepatocellular carcinoma pathogenesis

Contact Info

Product

Resources

About