Role of gga-miR-221 and gga-miR-222 during Tumour Formation in Chickens Infected by Subgroup J Avian Leukosis Virus

• Published in: Viruses Vol. 7; no. 12; pp. 6538 - 6551
• Main Authors: Dai, Zhenkai, Ji, Jun, Yan, Yiming, Lin, Wencheng, Li, Hongxin, Chen, Feng, Liu, Yang, Chen, Weiguo, Bi, Yingzuo, Xie, Qingmei
• Format: Journal Article
• Language: English
• Published: Switzerland MDPI 11.12.2015; MDPI AG
• Subjects: Animals; Apoptosis; Avian Leukosis - pathology; Avian Leukosis - virology; Avian Leukosis Virus - growth & development; BMF; cancer; Carcinogenesis; Cell Line; Cell Movement; Cell Proliferation; Chickens; cisplatin; doxorubicin; Gene Expression Profiling; gga-miR-221; gga-miR-222; Host-Pathogen Interactions; Liver - pathology; MicroRNAs - metabolism; subgroup J avian leukosis virus; subgroup J avian leukosis virus; apoptosis; BMF; cancer; doxorubicin; cisplatin; gga-miR-221; gga-miR-222
• ISSN: 1999-4915; 1999-4915
• DOI: 10.3390/v7122956

Subgroup J avian leukosis virus (ALV-J) causes a neoplastic disease in infected chickens. Differential expression patterns of microRNAs (miRNAs) are closely related to the formation and growth of tumors. (1) BACKGROUND: This study was undertaken to understand how miRNAs might be related to tumor growth during ALV-J infection. We chose to characterize the effects of miR-221 and miR-222 on cell proliferation, migration, and apoptosis based on previous microarray data. (2) METHODS: In vivo, the expression levels of miR-221 and miR-222 were significantly increased in the liver of ALV-J infected chickens (p < 0.01). Over-expression of gga-miR-221 and gga-miR-222 promoted the proliferation, migration, and growth of DF-1 cells, and decreased the expression of BCL-2 modifying factor (BMF) making cells more resistant to apoptosis. (3) RESULTS: Our results suggest that gga-miR-221 and gga-miR-222 may be tumour formation relevant gene in chicken that promote proliferation, migration, and growth of cancer cells, and inhibit apoptosis. BMF expression was significantly reduced in vivo 70 days after ALV-J infection. They may also play a pivotal role in tumorigenesis during ALV-J infection.