A Unilateral Negative Feedback Loop Between<i>miR-200</i>microRNAs and Sox2/E2F3 Controls Neural Progenitor Cell-Cycle Exit and Differentiation

Peng, Changgeng; Li, Na; Ng, Yen-Kar; Zhang, Jingzhong; Meier, Florian; Theis, Fabian J.; Merkenschlager, Matthias; Chen, Wei; Wurst, Wolfgang; Prakash, Nilima

doi:10.1523/jneurosci.2124-12.2012

Cited by 90 publications

(88 citation statements)

References 64 publications

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“…43 MiR-200 targets Sox2 and E2F3 while directly regulating miR-200 to form a feed-back circle to controls neural progenitor cell-cycle exit and differentiation. 44 In our study, miR-432 is also shown to inhibit proliferation by targeting E2F3. P55PIK, a regulatory subunit of PI3K, was identified to promote cell growth and cell proliferation 45,46 and interacted with proliferation cell nuclear antigen (PCNA) 25 to stimulate DNA synthesis.…”

Section: Discussionsupporting

confidence: 54%

MicroRNA-432 targeting E2F3 and P55PIK inhibits myogenesis through PI3K/AKT/mTOR signaling pathway

Wang

Chen

et al. 2017

RNA Biology

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Skeletal muscle is the dominant executant in locomotion and regulator in energy metabolism. Embryonic myogenesis and postnatal muscle growth are controlled by a cascade of transcription factors and epigenetic regulatory mechanisms. MicroRNAs (miRNAs), a family of non-coding RNA of 22 nucleotides in length, post-transcriptionally regulates expression of mRNA by pairing the seed sequence to 3 0 UTR of target mRNA. Increasing evidence has demonstrated that miRNAs are important regulators in diverse myogenic processes. The profiling of miRNA expression revealed that miR-432 is more enriched in the longissimus dorsi of 35-day-old piglets than that of adult pigs. Our gain of function study showed that miR-432 can negatively regulate both myoblast proliferation and differentiation. Mechanically, we found that miR-432 is able to down-regulate E2F transcription factor 3 (E2F3) to inactivate the expression of cell cycle and myogenic genes. We also identified that phosphatidylinositol 3-kinase regulatory subunit (P55PIK) is another target gene of miR-432 in muscle cells. downregulation of P55PIK by miR-432 leads to inhibition of P55PIK-mediated PI3K/AKT/mTOR signaling pathway during differentiation. The blocking effect of miR-432 on this pathway can be rescued by insulin treatment. Taken together, our findings identified microRNA-432 as a potent inhibitor of myogenesis which functions by targeting E2F3 and P55PIK in muscle cells.

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Section: Discussionsupporting

confidence: 54%

MicroRNA-432 targeting E2F3 and P55PIK inhibits myogenesis through PI3K/AKT/mTOR signaling pathway

Wang

Chen

et al. 2017

RNA Biology

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“…2L,M) at wild-type levels, strongly indicating that TRBP enhancement of Notch pathway activation is Dicer independent. Previous studies also support our observations: the expression of Hes genes was not altered in Dicer-ablated embryonic brains (Peng et al, 2012), and neural progenitors lacking Dicer did not precociously exit the VZ and still retained progenitor marker expression in vivo (Knuckles et al, 2012).…”

Section: Stem Cells and Regenerationsupporting

confidence: 90%

TRBP maintains mammalian embryonic neural stem cell properties by enhancing the Notch signaling pathway as a novel transcriptional coactivator

et al. 2017

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Transactivation response element RNA-binding protein (TRBP) is known to play important roles in human immunodeficiency virus (HIV) replication and microRNA biogenesis. However, recent studies implicate TRBP in a variety of biological processes as a mediator for cross-talk between signal transduction pathways. Here, we provide the first evidence that TRBP is required for efficient neurosphere formation, and expression of neural stem cell markers and Notch target genes in primary neural progenitor cells in vitro. Consistent with this, introduction of TRBP into the mouse embryonic brain in utero increased the fraction of cells expressing Sox2 in the ventricular zone (VZ). We also show TRBP physically interacts with the Notch transcriptional coactivation complex through C promoter binding factor 1 (CBF1) and strengthens the association between the Notch intracellular domain (NICD) and CBF1, resulting in increased NICD recruitment to the promoter region of a Notch target gene. Our data indicate that TRBP is a novel transcriptional coactivator of the Notch signaling pathway playing an important role in neural stem cell regulation during mammalian brain development.

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“…Sox2, occupying the promoters of miR-200c, in turn decreased expression of miR-200c; such a loop might well lead to the reactivation of Sox2. In a previous report, a miR-200c-Sox2 feedback loop contributed to cell-cycle exit and the neuronal differentiation of neural stem/progenitor cells (24). During induced pluripotent stem cell (iPSC) reprogramming in mouse embryonic fibroblasts, Oct4 specifically activates the mir-141/200c cluster and Sox2 specifically activates the mir-200a/b/429 cluster by binding to their promoters (41).…”

Section: Discussionmentioning

confidence: 97%

Regulation of Colorectal Carcinoma Stemness, Growth, and Metastasis by an miR-200c-Sox2–Negative Feedback Loop Mechanism

Xue

et al. 2014

Clinical Cancer Research

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Purpose: To elucidate a novel mechanism of miR-200c in the regulation of stemness, growth, and metastasis in colorectal carcinoma (CRC).Experimental Design: Quantitative reverse transcription PCR was used to quantify miR-200c expression in CRC cell lines and tissues. A luciferase assay was adopted for the target evaluation. The functional effects of miR-200c in CRC cells were assessed by its forced or inhibited expression using lentiviruses.Results :

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A Unilateral Negative Feedback Loop BetweenmiR-200microRNAs and Sox2/E2F3 Controls Neural Progenitor Cell-Cycle Exit and Differentiation

Cited by 90 publications

References 64 publications

MicroRNA-432 targeting E2F3 and P55PIK inhibits myogenesis through PI3K/AKT/mTOR signaling pathway

MicroRNA-432 targeting E2F3 and P55PIK inhibits myogenesis through PI3K/AKT/mTOR signaling pathway

TRBP maintains mammalian embryonic neural stem cell properties by enhancing the Notch signaling pathway as a novel transcriptional coactivator

Regulation of Colorectal Carcinoma Stemness, Growth, and Metastasis by an miR-200c-Sox2–Negative Feedback Loop Mechanism

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