Chicken gga-miR-130a targets HOXA3 and MDFIC and inhibits Marek’s disease lymphoma cell proliferation and migration

Han, Bo; Lian, Ling; Li, Xin; Zhao, Chunfang; Qu, Lujiang; Liu, Changjun; Song, Jiuzhou; Yang, Ning

doi:10.1007/s11033-016-4002-2

Cited by 20 publications

(11 citation statements)

References 78 publications

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“…Gga-miR-130a targets homeobox A3 (HOXA3) and MyoD family inhibitor domain containing (MDFIC), and gga-miR-103-3p targets cyclin E1 (CCNE1) and transcription factor Dp-2 (TFDP2). Both gga-miR-130a and gga-miR-103-3p inhibit proliferation of MSB1 cells 15, 16 . For viral miRNAs, Burnside et al .…”

Section: Introductionmentioning

confidence: 99%

Gga-miR-219b targeting BCL11B suppresses proliferation, migration and invasion of Marek’s disease tumor cell MSB1

Zhao

Han

et al. 2017

Sci Rep

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Marek’s disease (MD), caused by Marek’s disease virus (MDV), is a lymphotropic neoplastic disease. Previous miRNAome analysis showed gga-miR-219b was significantly downregulated in MDV-induced lymphoma, and one of its potential target genes, B-cell chronic lymphocytic /lymphoma 11B (BCL11B) was predicted. In this study, we further investigated the function of gga-miR-219b, and the gain/loss of function assay showed gga-miR-219b inhibited cell migration and reduced cell proliferation by promoting apoptosis not by cell cycle arrest. Gga-miR-219b also suppressed expression of two cell invasion-related genes MMP2 and MMP9. The results indicated suppressive effect of gga-miR-219b on MD tumorigenesis. The gene BCL11B was verified as a direct target gene of gga-miR-219b. RNA interference was performed to block BCL11B. As expected, the effects triggered by BCL11B downregulation were in accordance with that triggered by gga-miR-219b overexpression, suggesting that BCL11B was a stimulative regulator of MD transformation. Moreover, both gga-miR-219b and BCL11B influenced the expression of Meq gene, the most important oncogene in MDV. Additionally, gene expression level of anti-apoptotic genes BCL2 and BCL2L1 was downregulated and pro-apoptotic gene TNFSF10 was upregulated in MSB1 cells with gga-miR-219b overexpression or BCL11B knockdown, which suggested gga-miR-219b promoted cell apoptosis via regulating gene expression in the apoptosis pathways.

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Section: Introductionmentioning

confidence: 99%

Gga-miR-219b targeting BCL11B suppresses proliferation, migration and invasion of Marek’s disease tumor cell MSB1

Zhao

Han

et al. 2017

Sci Rep

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“…Several miRNAs, such as miR-27a, miR-30, miR-130b, and miR-146, attracted our attention because their expression changed significantly upon IBDV infection and they had been reported to participate in the immune response (16,(34)(35)(36)(37). We focused on the role of miR-130b in the cell response to IBDV infection because this miRNA participated in the antiviral process (38)(39)(40).…”

Section: Resultsmentioning

confidence: 99%

MicroRNA gga-miR-130b Suppresses Infectious Bursal Disease Virus Replication via Targeting of the Viral Genome and Cellular Suppressors of Cytokine Signaling 5

Wang

Chen

et al. 2018

J Virol

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MicroRNAs (miRNAs) are small noncoding RNAs that regulate gene expression posttranscriptionally through silencing or degrading their targets, thus playing important roles in the immune response. However, the role of miRNAs in the host response against infectious bursal disease virus (IBDV) infection is not clear. In this study, we show that the expression of a series of miRNAs was significantly altered in DF-1 cells after IBDV infection. We found that the miRNA gga-miR-130b inhibited IBDV replication via targeting the specific sequence of IBDV segment A and enhanced the expression of beta interferon (IFN-β) by targeting suppressors of cytokine signaling 5 (SOCS5) in host cells. These findings indicate that gga-miR-130b-3p plays a crucial role in host defense against IBDV infection. This work shows that gga-miR-130b suppresses IBDV replication via directly targeting the viral genome and cellular SOCS5, the negative regulator for type I interferon expression, revealing the mechanism underlying gga-miR-130-induced inhibition of IBDV replication. This information will be helpful for the understanding of how host cells combat pathogenic infection by self-encoded small RNA and furthers our knowledge of the role of microRNAs in the cell response to viral infection.

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“…Similarly to FOXP2, it interacts with LEF1, as part of beta-catenin regulation (Kusano et al 2002). In chicken MDFIC is targeted by miR-130a (Han et al 2016), known to regulate neurite outgrowth and dendritic spine density by targeting MeCP2, the main candidate for Rett syndrome, a condition involving language deficits (Zhang et al 2016). MDFIC is highly expressed in the cerebellum during human embryonic development and in the thalamus after birth (Human Brain Transcriptome http://hbatlas.org/).…”

Section: Discussionmentioning

confidence: 99%

Functional genetic characterization by CRISPR-Cas9 of two enhancers ofFOXP2in a child with speech and language impairment

Torres-Ruíz¹,

Benítez‐Burraco

Martínez-Lage³

et al. 2016

Preprint

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Mutations in the coding region of FOXP2 are known to cause speech and language impairment.Microdeletions involving the region downstream the gene have been also associated to speech and cognitive deficits. We recently described a girl harbouring a complex chromosomal rearrangement with one breakpoint downstream the gene that might affect their speech and cognitive abilities via physical separation of distant regulatory DNA elements. In this study, we have used highly efficient targeted chromosomal deletions induced by the CRISPR/Cas9 genome editing tool to demonstrate the functionality of two enhancers (FOXP2-E proximal and FOXP2-E distal ) located in the intergenic region between FOXP2 and its adjacent MDFIC gene. Deletion of any of these two functional enhancers in the neuroblastomic cell line SK-N-MC downregulates FOXP2 and decreases FOXP2 protein levels, conversely it upregulates MDFIC and increases MDFIC protein levels. This suggests that both regulatory elements may be shared between FOXP2 and MDFIC. We expect these findings contribute to a deeper understanding of how FOXP2 and MDFIC are regulated to pace neuronal development supporting speech and language. KEYWORDSFOXP2, MDFIC, speech and language impairment, Spanish, CRISP-Cas9, functional enhancer

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Chicken gga-miR-130a targets HOXA3 and MDFIC and inhibits Marek’s disease lymphoma cell proliferation and migration

Cited by 20 publications

References 78 publications

Gga-miR-219b targeting BCL11B suppresses proliferation, migration and invasion of Marek’s disease tumor cell MSB1

Gga-miR-219b targeting BCL11B suppresses proliferation, migration and invasion of Marek’s disease tumor cell MSB1

MicroRNA gga-miR-130b Suppresses Infectious Bursal Disease Virus Replication via Targeting of the Viral Genome and Cellular Suppressors of Cytokine Signaling 5

Functional genetic characterization by CRISPR-Cas9 of two enhancers ofFOXP2in a child with speech and language impairment

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