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Biochem Biophys Res Commun. 2016 Sep 30;478(4):1758-63. doi: 10.1016/j.bbrc.2016.09.020. Epub 2016 Sep 6.

Identification of miR-125b targets involved in acute promyelocytic leukemia cell proliferation.

Author information

1
Institute of Hematology, Medical College, Jinan University, Guangzhou, 510632, China; Key Laboratory for Regenerative Medicine of Ministry of Education, Jinan University, Guangzhou, 510632, China; First Affiliated Hospital, Jinan University, Guangzhou 510632, China.
2
Institute of Hematology, Medical College, Jinan University, Guangzhou, 510632, China; Key Laboratory for Regenerative Medicine of Ministry of Education, Jinan University, Guangzhou, 510632, China; First Affiliated Hospital, Jinan University, Guangzhou 510632, China. Electronic address: bio-zcw@163.com.
3
Institute of Hematology, Medical College, Jinan University, Guangzhou, 510632, China; Key Laboratory for Regenerative Medicine of Ministry of Education, Jinan University, Guangzhou, 510632, China.
4
Institute of Hematology, Medical College, Jinan University, Guangzhou, 510632, China.
5
First Affiliated Hospital, Jinan University, Guangzhou 510632, China.
6
Institute of Hematology, Medical College, Jinan University, Guangzhou, 510632, China; Key Laboratory for Regenerative Medicine of Ministry of Education, Jinan University, Guangzhou, 510632, China; First Affiliated Hospital, Jinan University, Guangzhou 510632, China. Electronic address: yangqiuli@hotmail.com.

Abstract

Acute promyelocytic leukemia (APL) is characterized by the presence of the PML-RARα fusion protein. We have previously found that PML-RARα-regulated miR-125b is highly expressed in APL; however, the characteristics of the regulatory effects and mechanisms of miR-125b involved in APL proliferation have yet to be clarified. In this study, we demonstrate that miR-125b promotes the proliferation of APL cells with the involvement of the PI3K/Akt and MAPK signaling pathways. Furthermore, we identified BTG2, MAP3K11, RPS6KA1 and PRDM1 as putative targets of miR-125b, which we verified using luciferase reporter constructs. Moreover, we demonstrate that the expression of miR-125b targets is downregulated in leukemic cells in patients with APL. Thus, our results provide evidence that miR-125b can modulate multiple oncogenic cell proliferation pathways and may be a novel therapeutic target for APL.

KEYWORDS:

3′-untranslated regions; Acute promyelocytic leukemia; MicroRNAs; PML-RARα; Proliferation; Small non-coding RNAs

PMID:
27613090
DOI:
10.1016/j.bbrc.2016.09.020
[Indexed for MEDLINE]

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