Imbalanced expression of polycistronic miRNA in acute myeloid leukemia

• Main Authors: Kotaki, Ryutaro, Higuchi, Hiroshi, Ogiya, Daisuke, Katahira, Yasuhiro, Kurosaki, Natsumi, Yukihira, Naoko, Ogata, Jun, Yamamoto, Haruna, Mohamad Alba, Syakira, Azhim, Azran, Kitajima, Tatsuo, Inoue, Shigeaki, Morishita, Kazuhiro, Ono, Koh, Koyama-Nasu, Ryo, Kotani, Ai
• Format: Article
• Language: English; English
• Published: Springer International Publishing AG 2017
• Subjects: RC0254 Neoplasms. Tumors. Oncology (including Cancer)
• Online Access: http://irep.iium.edu.my/58944/1/10.1007%40s12185-017-2314-1.pdf; http://irep.iium.edu.my/58944/7/Imbalanced%20expression%20of%20polycistronic%20miRNA%20in%20acute%20myeloid%20leukemia.pdf; http://irep.iium.edu.my/58944/; https://link.springer.com/article/10.1007/s12185-017-2314-1

miR-1 and miR-133 are clustered on the same chromosomal loci and are transcribed together as a single transcript that is positively regulated by ecotropic virus integration site-1 (EVI1). Previously, we described how miR-133 has anti-tumorigenic potential through repression of EVI1 expression. It has also been reported that miR-1 is oncogenic in the case of acute myeloid leukemia (AML). Here, we show that expression of miR-1 and miR-133, which have distinct functions, is differentially regulated between AML cell lines. Interestingly, the expression of miR-1 and EVI1, which binds to the promoter of the miR-1/miR-133 cluster, is correlative. The expression levels of TDP-43, an RNA-binding protein that has been reported to increase the expression, but inhibits the activity, of miR-1, were not correlated with expression levels of miR-1 in AML cells. Taken together, our observations raise the possibility that the balance of polycistronic miRNAs is regulated post-transcriptionally in a hierarchical manner possibly involving EVI1,suggesting that the deregulation of this balance may play some role in AML cells with high EVI1 expression.