FosB regulates expression of miR-22 during PMA induced differentiation of K562 cells to megakaryocytes

Muiwo, Pamchui; Muthuswami, Rohini; Bhattacharya, Alok

doi:10.1016/j.biochi.2016.11.005

Cited by 14 publications

(15 citation statements)

References 33 publications

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“…Besides, many transcription factors are responsible for the regulation of miR22 expression. Some studies confirmed the genes FosB, c-Fos, PU.1, P53, NFκB, and AKT as the transcription regulators of miR22 in different cells 10 , 15 , 27 , 32 – 34 . However, RPL29 is not a transcription factor of miR22.…”

Section: Resultsmentioning

confidence: 89%

“…Recent numerous studies confirmed that the expression of miR22 is regulated transcriptionally along with its host gene by some transcription factors including NF-κB, p53, Fos-B, c-Fos, PU.1, AKT Jak3, STAT3, and STAT5 10,15,27,[32][33][34]41 . There are some cellular and extracellular stimuli including polyinosinic-polycytidylic acid (poly(I:C)), phorbol-12-myristate-13-acetate, endosulfan, IL1α, nicotinamide phosphoribosyltransferase, 12-o-tetradecanoylphorbol-13-acetate, and xendin-4 those regulate the expression of miR-22 5,13,16,20,26,27 . In addition, HIP/RPL29 expression www.nature.com/scientificreports/ is regulated by both sodium butyrate and glucose deprivation in HT-29 cells and results in induction of cellular differentiation 42 .…”

Section: Discussionmentioning

confidence: 96%

“…Collectively these results indicated that the poly(I:C) induced differential expression of miR22 in the mouse lung and brain tissues and in the glial and endothelial cells might be regulated by RPL29. Recent numerous studies confirmed that the expression of miR22 is regulated transcriptionally along with its host gene by some transcription factors including NF-κB, p53, Fos-B, c-Fos, PU.1, AKT Jak3, STAT3, and STAT5 10 , 15 , 27 , 32 – 34 , 41 . There are some cellular and extracellular stimuli including polyinosinic-polycytidylic acid (poly(I:C)), phorbol-12-myristate-13-acetate, endosulfan, IL1α, nicotinamide phosphoribosyltransferase, 12-o-tetradecanoylphorbol-13-acetate, and xendin-4 those regulate the expression of miR-22 5 , 13 , 16 , 20 , 26 , 27 .…”

Section: Discussionmentioning

confidence: 96%

“…Besides these, RPL29 knockdown results in the down expression of Fos-B and c-Fos in these two cell lines. The Fos-B and c-Fos are two experimentally validated transcription factors of miR22 27,32 . These findings suggested that the RPL29 might regulate the expression of miR22 through the transcriptional activities of the AP-1 protein family members Fos-B and c-Fos.…”

Section: Discussionmentioning

confidence: 99%

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The tissue specific regulation of miR22 expression in the lung and brain by ribosomal protein L29

Ali

et al. 2020

Sci Rep

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Endogenous miR22 is associated with a diverse range of biological processes through post-translational modification of gene expression and its deregulation results in various diseases including cancer. Its expression is usually tissue or cell-specific, however, the reasons behind this tissue or cell specificity are not clearly outlined till-date. Therefore, our keen interest was to investigate the mechanisms of tissue or cell-specific expression of miR22. In the current study, miR22 expression showed a tissues-specific difference in the poly(I:C) induced inflammatory mouse lung and brain tissues. The cell-specific different expression of miR22 was also observed in inflammatory glial cells and endothelial cells. The pattern of RPL29 expression was also similar to miR22 in these tissues and cells under the same treatment. Interestingly, the knockdown of RPL29 exerted an inhibitory effect on miR22 and its known transcription factors including Fos-B and c-Fos. Fos-B and c-Fos were also differentially expressed in the two cell lines transfected with poly(I:C). The knockdown of c-Fos also exerted its negative effects on miR22 expression in both cells. These findings suggest that RPL29 might have regulatory roles on tissue or cell-specific expression of miR22 through the transcription activities of c-Fos and also possibly through Fos-B.

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Section: Resultsmentioning

confidence: 89%

Section: Discussionmentioning

confidence: 96%

Section: Discussionmentioning

confidence: 96%

Section: Discussionmentioning

confidence: 99%

See 2 more Smart Citations

The tissue specific regulation of miR22 expression in the lung and brain by ribosomal protein L29

Ali

et al. 2020

Sci Rep

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“…Recent studies have shown that the transcription factors of miR-22 include Jak3, STAT3, STAT5, and FosB. FosB promotes the expression of miR-22, while Jak3, STAT3, and STAT5 are transcriptional repressors[35,36]. In this study, to identify the miR-22 transcription factor involved in regulating the apoptosis of pancreatic acinar cells, we first predicted the transcription factor and TSS.…”

Section: Discussionmentioning

confidence: 99%

Glucocorticoid receptor regulates expression of microRNA-22 and downstream signaling pathway in apoptosis of pancreatic acinar cells

Liu

et al. 2018

WJG

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AIMTo elucidate the underlying mechanism that microRNA-22 (miR-22) promotes the apoptosis of rat pancreatic acinar cells (AR42J) and the elements that regulate the expression of miR-22.METHODSOne hundred nanomoles per liter of caerulein (Cae) was administrated to induce the apoptosis of AR42J cells and the apoptosis rate was detected by flow cytometry analysis. An amylase assay kit was used to measure the amylase expression level in the supernatant. Quantitative real-time PCR (qRT-PCR) was adopted to measure miR-22 expression. We used online tools to predict the potential transcription promoter of miR-22 and the binding sites, which was further identified by using luciferase reporter analysis, chromatin immunoprecipitation (ChIP) and ChIP-qPCR assays. Then, a mimic of miR-22, Nr3c1 plasmid encoding the glucocorticoid receptor (GR), and si-Nr3c1 were used to transfect AR42J cells, respectively. The mRNA expression of miR-22, Nr3c1, and Erb-b2 receptor tyrosine kinase 3 (ErbB3) was confirmed by qRT-PCR and the apoptosis rate of AR42J cells was detected by flow cytometry analysis. Western blot was used to detect the expression of ErbB3, GR, PI3k, PI3k-p85α, Akt, p-Akt, Bad, Bax, Bcl-xl, Bcl-2, and cleaved caspase3.RESULTSAfter inducing apoptosis of AR42J cells in vitro, the expression of miR-22 was significantly increased by 2.20 ± 0.26 and 4.19 ± 0.54 times, respectively, at 3 h and 6 h in comparison with the control group. As revealed by qRT-PCR assay, the expression of miR-22 was 78.25 ± 6.61 times higher in the miR-22 mimic group relative to the miRNA control group, accompanied with an obviously increased acinar cell apoptosis rate (32.53 ± 1.15 vs 18.07 ± 0.89, P = 0.0006). The upregulation of miR-22 could suppress its target gene, ErbB3, and the phosphorylation of PI3k and Akt. Furthermore, we predicted the potential transcription promoter of miR-22 and the binding sites using online tools. Luciferase reporter analysis and site-directed mutagenesis indicated that the binding site (GACAGCCATGTACA) of the GR, which is encoded by the Nr3c1 gene. Downregulation of the expression of GR could upregulate the expression of miR-22, which further promoted the apoptosis of AR42J cells.CONCLUSIONGR transcriptionally represses the expression of miR-22, which further promotes the apoptosis of pancreatic acinar cells by downregulating the downstream signaling pathway.

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MicroRNAs as regulators and effectors of hematopoietic transcription factors

2019

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Hematopoiesis is a highly-regulated development process orchestrated by lineagespecific transcription factors that direct the generation of all mature blood cells types, including red blood cells, megakaryocytes, granulocytes, monocytes, and lymphocytes. Under homeostatic conditions, the hematopoietic system of the typical adult generates over 10 11 blood cells daily throughout life. In addition, hematopoiesis must be responsive to acute challenges due to blood loss or infection. MicroRNAs (miRs) cooperate with transcription factors to regulate all aspects of hematopoiesis, including stem cell maintenance, lineage selection, cell expansion, and terminal differentiation. Distinct miR expression patterns are associated with specific hematopoietic lineages and stages of differentiation and functional analyses have elucidated essential roles for miRs in regulating cell transitions, lineage selection, maturation, and function. MiRs function as downstream effectors of hematopoietic transcription factors and as upstream regulators to control transcription factor levels. Multiple miRs have been shown to play essential roles. Regulatory networks comprised of differentially expressed lineage-specific miRs and hematopoietic transcription factors are involved in controlling the quiescence and self-renewal of hematopoietic stem cells as well as proliferation and differentiation of lineage-specific progenitor cells during erythropoiesis, myelopoiesis, and lymphopoiesis. This review focuses on hematopoietic miRs that function as upstream regulators of central hematopoietic transcription factors required for normal hematopoiesis.

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FosB regulates expression of miR-22 during PMA induced differentiation of K562 cells to megakaryocytes

Cited by 14 publications

References 33 publications

The tissue specific regulation of miR22 expression in the lung and brain by ribosomal protein L29

The tissue specific regulation of miR22 expression in the lung and brain by ribosomal protein L29

Glucocorticoid receptor regulates expression of microRNA-22 and downstream signaling pathway in apoptosis of pancreatic acinar cells

MicroRNAs as regulators and effectors of hematopoietic transcription factors

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