The Silencing Effect of microRNA miR-17 on p21 Maintains the Neural Progenitor Pool in the Developing Cerebral Cortex

Chen, Yase; Bian, Shan; Zhang, Jing; Zhang, Haijun; Tang, Beisha; Sun, Tao

doi:10.3389/fneur.2014.00132

Cited by 17 publications

(12 citation statements)

References 43 publications

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“…2). Garg et al and our group both observed that miR-17/106 sub-family miRNAs (miR-17, miR-20, and miR-106) target key components of p53 signaling, Trp53inp1 and p21 [26,27,39]. TSG101-Trp53inp1-p53-p21 is a key axis in modulating cell growth arrest and apoptosis [50].…”

Section: The Regulatory Network Of Mir-17~92 Familymentioning

confidence: 76%

“…After that, the roles of individual miR-17~92 family miRNA in the regulation of NSCs were examined. The ectopic expression of miR-17 or miR-106b, two miR-17/106 sub-family miRNAs, enhances the proliferation of embryonic cortical NSCs, therefore maintains the NSC pool in the developing cerebral cortex [26,38,39]. The knockdown of miR-17 and miR-20, by contrast, significantly inhibits the proliferation of mouse cerebella NSCs, ascertained by EdU incorporation assay, neurosphere counting, and FACS-based cell cycle analysis [27].…”

Section: Mir-17~92 Family In Developmental Neurogenesismentioning

confidence: 99%

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The microRNA-17 ~ 92 Family as a Key Regulator of Neurogenesis and Potential Regenerative Therapeutics of Neurological Disorders

Xia

Wang

Zheng

2020

Stem Cell Rev and Rep

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miR-17 ~ 92, an miRNA family containing three paralogous polycistronic clusters, was initially considered as an oncogene and was later demonstrated to trigger various physiological and pathological processes. Emerging evidence has implicated miR-17 ~ 92 family as a master regulator of neurogenesis. Through targeting numerous genes that affect cell cycle arrest, stemness deprivation, and lineage commitment, miR-17 ~ 92 family controls the proliferation and neuronal differentiation of neural stem/progenitor cells in both developmental and adult brains. Due to the essential roles of miR-17 ~ 92 family, its misexpression is widely associated with acute and chronic neurological disorders by attenuating neurogenesis and facilitating neuronal apoptosis. The promising neurogenic potential of miR-17 ~ 92 family also makes it a promising “medicine” to activate the endogenous and exogenous regenerative machinery, thus enhance tissue repair and function recovery after brain injury. In this review, we focus on the recent progress made toward understanding the involvement of miR-17 ~ 92 family in regulating both developmental and adult neurogenesis, and discuss the regenerative potential of miR-17 ~ 92 family in treating neurological disorders.

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Section: The Regulatory Network Of Mir-17~92 Familymentioning

confidence: 76%

Section: Mir-17~92 Family In Developmental Neurogenesismentioning

confidence: 99%

The microRNA-17 ~ 92 Family as a Key Regulator of Neurogenesis and Potential Regenerative Therapeutics of Neurological Disorders

Xia

Wang

Zheng

2020

Stem Cell Rev and Rep

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“…Previous studies of developing neocortex have shown that miRs in the miR-17-92 cluster prevent the transition from RGPs to IPs, in part by targeting Tbr2 and Cdkn1a (p21) (Bian et al, 2013 ; Chen et al, 2014 ). Within the cluster, miR-92a was found to target Tbr2 (Bian et al, 2013 ).…”

Section: Resultsmentioning

confidence: 99%

The Epigenetic Factor Landscape of Developing Neocortex Is Regulated by Transcription Factors Pax6→ Tbr2→ Tbr1

Elsen¹,

Bedogni²,

Hodge³

et al. 2018

Front. Neurosci.

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Epigenetic factors (EFs) regulate multiple aspects of cerebral cortex development, including proliferation, differentiation, laminar fate, and regional identity. The same neurodevelopmental processes are also regulated by transcription factors (TFs), notably the Pax6→ Tbr2→ Tbr1 cascade expressed sequentially in radial glial progenitors (RGPs), intermediate progenitors, and postmitotic projection neurons, respectively. Here, we studied the EF landscape and its regulation in embryonic mouse neocortex. Microarray and in situ hybridization assays revealed that many EF genes are expressed in specific cortical cell types, such as intermediate progenitors, or in rostrocaudal gradients. Furthermore, many EF genes are directly bound and transcriptionally regulated by Pax6, Tbr2, or Tbr1, as determined by chromatin immunoprecipitation-sequencing and gene expression analysis of TF mutant cortices. Our analysis demonstrated that Pax6, Tbr2, and Tbr1 form a direct feedforward genetic cascade, with direct feedback repression. Results also revealed that each TF regulates multiple EF genes that control DNA methylation, histone marks, chromatin remodeling, and non-coding RNA. For example, Tbr1 activates Rybp and Auts2 to promote the formation of non-canonical Polycomb repressive complex 1 (PRC1). Also, Pax6, Tbr2, and Tbr1 collectively drive massive changes in the subunit isoform composition of BAF chromatin remodeling complexes during differentiation: for example, a novel switch from Bcl7c (Baf40c) to Bcl7a (Baf40a), the latter directly activated by Tbr2. Of 11 subunits predominantly in neuronal BAF, 7 were transcriptionally activated by Pax6, Tbr2, or Tbr1. Using EFs, Pax6→ Tbr2→ Tbr1 effect persistent changes of gene expression in cell lineages, to propagate features such as regional and laminar identity from progenitors to neurons.

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“…MiR‐17 has been elucidated to target p21 in other contexts including some cancers. MiR‐17 promotes the developing cortex through suppressing p21 expression for maintaining the neural progenitor pool . Overexpression of miR‐17‐5p promotes cell growth in chronic myelogenous leukemia and B‐cell lymphoma cell lines by targeting p21 .…”

Section: Introductionmentioning

confidence: 99%

MiR‐17‐5p promotes cancer cell proliferation and tumorigenesis in nasopharyngeal carcinoma by targeting p21

Chen

Yang

et al. 2016

Cancer Medicine

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MicroRNAs (miRNAs) may act as either tumor suppressors or oncogenes in various types of cancers. Previous studies have indicated that miR‐17‐5p is involved in the initiation and development of human tumors. However, its mechanism and function in nasopharyngeal carcinoma (NPC) remain largely unclear. In this study, we evaluated the expression profiles of miR‐17‐5p and p21 in NPC cell lines and tissues by quantitative real‐time PCR (qRT‐PCR). For the analysis, we have established a stable overexpression or depletion of miR‐17‐5p NPC cell lines for analyzing the effects of cell proliferation by MTT, colony formation, and cell cycle assay. A nude mice xenograft model was used to verify the tumor growth in vivo. MiR‐17‐5p was overexpressed, whereas the expression of p21 was downregulated in NPC cell lines and tissues. The miR‐17‐5p expression level was inversely correlated with the p21 mRNA level in NPC samples. Furthermore, analysis of 2−ΔΔCt value in 81 NPC patients suggested that the elevated expression level of miR‐17‐5p or the downregulated expression level of p21 was significantly correlated with tumor size (T classification) and tumor stage, and Kaplan–Meier survival analysis revealed a correlation between miR‐17‐5p or p21 expression level and overall survival times in 81 NPC patients. MiR‐17‐5p promoted cell growth in vivo and in vitro by directly targeting p21. Our results indicate that miR‐17‐5p can promote the occurrence of NPC and it may serve as a potential novel diagnostic maker or therapeutic target for NPC in the future.

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The Silencing Effect of microRNA miR-17 on p21 Maintains the Neural Progenitor Pool in the Developing Cerebral Cortex

Cited by 17 publications

References 43 publications

The microRNA-17 ~ 92 Family as a Key Regulator of Neurogenesis and Potential Regenerative Therapeutics of Neurological Disorders

The microRNA-17 ~ 92 Family as a Key Regulator of Neurogenesis and Potential Regenerative Therapeutics of Neurological Disorders

The Epigenetic Factor Landscape of Developing Neocortex Is Regulated by Transcription Factors Pax6→ Tbr2→ Tbr1

MiR‐17‐5p promotes cancer cell proliferation and tumorigenesis in nasopharyngeal carcinoma by targeting p21

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