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

Abstract 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)...

Descripción completa

Guardado en:
Detalles Bibliográficos
Autores principales: Chunfang Zhao, Xin Li, Bo Han, Zhen You, Lujiang Qu, Changjun Liu, Jiuzhou Song, Ling Lian, Ning Yang
Formato: article
Lenguaje:EN
Publicado: Nature Portfolio 2017
Materias:
R
Q
Acceso en línea:https://doaj.org/article/89f546ac085e442094a60b612f3db1c8
Etiquetas: Agregar Etiqueta
Sin Etiquetas, Sea el primero en etiquetar este registro!
id oai:doaj.org-article:89f546ac085e442094a60b612f3db1c8
record_format dspace
spelling oai:doaj.org-article:89f546ac085e442094a60b612f3db1c82021-12-02T16:06:06ZGga-miR-219b targeting BCL11B suppresses proliferation, migration and invasion of Marek’s disease tumor cell MSB110.1038/s41598-017-04434-w2045-2322https://doaj.org/article/89f546ac085e442094a60b612f3db1c82017-06-01T00:00:00Zhttps://doi.org/10.1038/s41598-017-04434-whttps://doaj.org/toc/2045-2322Abstract 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.Chunfang ZhaoXin LiBo HanZhen YouLujiang QuChangjun LiuJiuzhou SongLing LianNing YangNature PortfolioarticleMedicineRScienceQENScientific Reports, Vol 7, Iss 1, Pp 1-12 (2017)
institution DOAJ
collection DOAJ
language EN
topic Medicine
R
Science
Q
spellingShingle Medicine
R
Science
Q
Chunfang Zhao
Xin Li
Bo Han
Zhen You
Lujiang Qu
Changjun Liu
Jiuzhou Song
Ling Lian
Ning Yang
Gga-miR-219b targeting BCL11B suppresses proliferation, migration and invasion of Marek’s disease tumor cell MSB1
description Abstract 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.
format article
author Chunfang Zhao
Xin Li
Bo Han
Zhen You
Lujiang Qu
Changjun Liu
Jiuzhou Song
Ling Lian
Ning Yang
author_facet Chunfang Zhao
Xin Li
Bo Han
Zhen You
Lujiang Qu
Changjun Liu
Jiuzhou Song
Ling Lian
Ning Yang
author_sort Chunfang Zhao
title Gga-miR-219b targeting BCL11B suppresses proliferation, migration and invasion of Marek’s disease tumor cell MSB1
title_short Gga-miR-219b targeting BCL11B suppresses proliferation, migration and invasion of Marek’s disease tumor cell MSB1
title_full Gga-miR-219b targeting BCL11B suppresses proliferation, migration and invasion of Marek’s disease tumor cell MSB1
title_fullStr Gga-miR-219b targeting BCL11B suppresses proliferation, migration and invasion of Marek’s disease tumor cell MSB1
title_full_unstemmed Gga-miR-219b targeting BCL11B suppresses proliferation, migration and invasion of Marek’s disease tumor cell MSB1
title_sort gga-mir-219b targeting bcl11b suppresses proliferation, migration and invasion of marek’s disease tumor cell msb1
publisher Nature Portfolio
publishDate 2017
url https://doaj.org/article/89f546ac085e442094a60b612f3db1c8
work_keys_str_mv AT chunfangzhao ggamir219btargetingbcl11bsuppressesproliferationmigrationandinvasionofmareksdiseasetumorcellmsb1
AT xinli ggamir219btargetingbcl11bsuppressesproliferationmigrationandinvasionofmareksdiseasetumorcellmsb1
AT bohan ggamir219btargetingbcl11bsuppressesproliferationmigrationandinvasionofmareksdiseasetumorcellmsb1
AT zhenyou ggamir219btargetingbcl11bsuppressesproliferationmigrationandinvasionofmareksdiseasetumorcellmsb1
AT lujiangqu ggamir219btargetingbcl11bsuppressesproliferationmigrationandinvasionofmareksdiseasetumorcellmsb1
AT changjunliu ggamir219btargetingbcl11bsuppressesproliferationmigrationandinvasionofmareksdiseasetumorcellmsb1
AT jiuzhousong ggamir219btargetingbcl11bsuppressesproliferationmigrationandinvasionofmareksdiseasetumorcellmsb1
AT linglian ggamir219btargetingbcl11bsuppressesproliferationmigrationandinvasionofmareksdiseasetumorcellmsb1
AT ningyang ggamir219btargetingbcl11bsuppressesproliferationmigrationandinvasionofmareksdiseasetumorcellmsb1
_version_ 1718385099743952896