miR-203 modulates epithelial differentiation of human embryonic stem cells towards epidermal stratification

Nissan, Xavier; Denis, Jérôme Alexandre; Saidani, Manoubia; Lemaı̂tre, Gilles; Peschanski, Marc; Baldeschi, Christine

doi:10.1016/j.ydbio.2011.06.004

Cited by 44 publications

(30 citation statements)

References 47 publications

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“…2C). Together, these data suggest that the miRNAs in the first two groups respond consistently to HPV18 infection; however, the responses of the host miRNAs in group 3 and group 4 to HPV18 infection appear to be regulated by HPV activities (7) and keratinocyte differentiation, as reported (31,32). Based on these results and on the data shown in Fig.…”

Section: Hpv18 Regulates Host Mirna Expression Over the Course Of Thesupporting

confidence: 59%

microRNAs are biomarkers of oncogenic human papillomavirus infections

Wang

et al. 2014

Proc. Natl. Acad. Sci. U.S.A.

175

177

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Cellular and viral microRNAs (miRNAs) are the transcriptional products of RNA polymerase II and are regulated by transcriptional factors for their differential expression. The altered expression of miRNAs in many cancer types has been explored as a marker for possible diagnosis and therapy. We report in this study that oncogenic human papillomaviruses (HPVs) induce aberrant expression of many cellular miRNAs and that HPV18 infection produces no detectable viral miRNA. Thirteen abundant host miRNAs were specifically regulated by HPV16 and HPV18 in organotypic raft cultures of foreskin and vaginal keratinocytes as determined by miRNA array in combination with small RNA sequencing. The increase of miR-16, miR-25, miR-92a, and miR-378 and the decrease of miR-22, miR-27a, miR-29a, and miR-100 could be attributed to viral oncoprotein E6, E7, or both, all of which are known to target many cellular transcription factors. The examination of 158 cervical specimens, including 38 normal, 52 cervical intraepithelial neoplasia (CIN), and 68 cervical cancer (CC) tissues, for the expression of these eight miRNAs showed a remarkable increase of miR-25, miR-92a, and miR-378 with lesion progression but no obvious change of miR-22, miR-29a, and miR-100 among the HPV-infected tissues. Further analyses indicate that an expression ratio ≥1.5 of miR-25/92a group over miR-22/29a group could serve as a cutoff value to distinguish normal cervix from CIN and from CIN to CC. oncogenes E6 and E7 | noncoding RNAs | regulatory RNAs | virol oncogenesis | DNA tumor viruses

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Section: Hpv18 Regulates Host Mirna Expression Over the Course Of Thesupporting

confidence: 59%

microRNAs are biomarkers of oncogenic human papillomavirus infections

Wang

et al. 2014

Proc. Natl. Acad. Sci. U.S.A.

175

177

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“…As with Let-7i, miR-203 has been shown to regulate proliferation (Chen et al ., 2013) and stem cell differentiation (Nissan et al ., 2011). In addition, miR-203 has been shown to be involved in epithelial-mesenchymal transdifferentiation (Ding et al ., 2013), a process thought to be critical for fusion of the facial processes (Jiang et al ., 2006).…”

Section: Discussionmentioning

confidence: 99%

MicroRNA expression profiling of the developing murine upper lip

et al. 2014

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Clefts of the lip and palate are thought to be caused by genetic and environmental insults but the role of epigenetic mechanisms underlying this common birth defect are unknown. We analyzed the expression of over 600 microRNAs in the murine medial nasal and maxillary processes isolated on GD10.0-GD11.5 to identify those expressed during development of the upper lip and analyzed spatial expression of a subset. A total of 169 microRNAs were differentially expressed across gestation days 10.0 to 11.5 in the medial nasal processes, and 77 in the maxillary processes of the first branchial arch with 49 common to both. Of the microRNAs exhibiting the largest percent increase in both facial processes were 5 members of the Let-7 family. Among those with the greatest decrease in expression from GD10.0 to GD11.5 were members of the microRNA-302/367 family that have been implicated in cellular reprogramming. The distribution of expression of microRNA-199a-3p and Let-7i was determined by in situ hybridization and revealed widespread expression in both medial nasal and maxillary facial processes while that for microRNA-203 was much more limited. MicroRNAs are dynamically expressed in the tissues that form the upper lip and several were identified that target mRNAs known to be important for its development, including those that regulate the two main isoforms of p63 (microRNA-203 and microRNA-302/367 family). Integration of these data with corresponding proteomic data sets will lead to a greater appreciation of epigenetic regulation of lip development and provide a better understanding of potential causes of cleft lip.

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“…Furthermore, several other studies provide evidence showing that Bmi1 plays a critical role in the maintenance of NSPC multipotency and proliferation in the forebrain (Fasano et al., 2009), and miR-203 has been previously suggested to play a unique role during the entire process of epidermal development by extending its spectrum of action from the early commitment of human embryonic stem cells to ultimate differentiation of the organ (Nissan et al., 2011). In this study, we provide evidence that the EZH2-miR-203-BMI1 regulatory axis exists in NSPCs.…”

Section: Discussionmentioning

confidence: 99%

MiR-203 Interplays with Polycomb Repressive Complexes to Regulate the Proliferation of Neural Stem/Progenitor Cells

Tang

et al. 2017

Stem Cell Reports

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SummaryThe polycomb repressive complexes 1 (PRC1) and 2 (PRC2) are two distinct polycomb group (PcG) proteins that maintain the stable silencing of specific sets of genes through chromatin modifications. Although the PRC2 component EZH2 has been known as an epigenetic regulator in promoting the proliferation of neural stem/progenitor cells (NSPCs), the regulatory network that controls this process remains largely unknown. Here we show that miR-203 is repressed by EZH2 in both embryonic and adult NSPCs. MiR-203 negatively regulates the proliferation of NSPCs. One of PRC1 components, Bmi1, is a downstream target of miR-203 in NSPCs. Conditional knockout of Ezh2 results in decreased proliferation ability of both embryonic and adult NSPCs. Meanwhile, ectopic overexpression of BMI1 rescues the proliferation defects exhibited by miR-203 overexpression or EZH2 deficiency in NSPCs. Therefore, this study provides evidence for coordinated function of the EZH2-miR-203-BMI1 regulatory axis that regulates the proliferation of NSPCs.

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miR-203 modulates epithelial differentiation of human embryonic stem cells towards epidermal stratification

Cited by 44 publications

References 47 publications

microRNAs are biomarkers of oncogenic human papillomavirus infections

microRNAs are biomarkers of oncogenic human papillomavirus infections

MicroRNA expression profiling of the developing murine upper lip

MiR-203 Interplays with Polycomb Repressive Complexes to Regulate the Proliferation of Neural Stem/Progenitor Cells

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