Literature DB >> 33686586

Gga-miR-181a modulates ANP32A expression and inhibits MDCC-MSB-1 cell.

X Li1,2, C Zhao1, B Han1, L Qu1, C Liu3, N Yang1, L Lian4.   

Abstract

Marek's disease (MD), a highly contagious T cell lymphoid neoplasia disease of chickens, causes huge economic losses to the poultry industry. It is the only one tumor disease which can be prevented by vaccine in chickens; therefore, MD is considered to be an excellent model to study the pathogenesis of virus-induced cancer. Recently, abundant evidences have verified that miRNAs are regulators in the process of neoplastic transformation. In our previous study on miRNome analysis of MDV-induced lymphoma in chicken, we found that gga-miR-181a was downregulated drastically in MDV-infected spleens. To further investigate the role of gga-miR-181a in MDV-induced lymphomagenesis, we performed cell migration assay, and the results suggested that gga-miR-181a suppressed the migration of MDV-transformed lymphoid cell (MSB-1). Subsequently, luciferase reporter gene assay revealed that acidic nuclear phosphoprotein 32A (ANP32A) was a functional target gene of gga-miR181a. Real-time PCR and western blot assay showed that the mRNA and protein levels of ANP32A were downregulated in gga-miR-181a mimic group at 48-h and 96-h post-transfection, respectively, indicating that ANP32A was modulated by gga-miR-181a. All the results suggested that gga-miR-181a was an inhibitor in MSB-1 cell migration. ANP32A was a direct target gene of gga-miR-181a and they were implicated in MD lymphoma tumorigenesis.

Entities:  

Keywords:  ANP32A; Chicken; Marek’s disease; gga-miR-181a

Year:  2021        PMID: 33686586     DOI: 10.1007/s11626-021-00550-0

Source DB:  PubMed          Journal:  In Vitro Cell Dev Biol Anim        ISSN: 1071-2690            Impact factor:   2.416


  47 in total

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10.  Fine mapping of QTL and genomic prediction using allele-specific expression SNPs demonstrates that the complex trait of genetic resistance to Marek's disease is predominantly determined by transcriptional regulation.

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