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miR-125a regulates cell cycle, proliferation, and apoptosis by targeting the ErbB pathway in acute myeloid leukemia.

Abstract：

:microRNA profiling of acute myeloid leukemia patient samples identified miR-125a as being decreased. Current literature has investigated miR-125a's role in normal hematopoiesis but not within acute myeloid leukemia. Analysis of the upstream region of miR-125a identified several CpG islands. Both precursor and mature miR-125a increased in response to a de-methylating agent, Decitabine. Profiling revealed the ErbB pathway as significantly decreased with ectopic miR-125a. Either ectopic expression of miR-125a or inhibition of ErbB via Mubritinib resulted in inhibition of cell cycle proliferation and progression with enhanced apoptosis revealing ErbB inhibitors as potential novel therapeutic agents for treating miR-125a-low AML.

journal_name

Leuk Res

journal_title

Leukemia research

authors

Ufkin ML,Peterson S,Yang X,Driscoll H,Duarte C,Sathyanarayana P

doi

10.1016/j.leukres.2013.12.021

subject

Has Abstract

pub_date

2014-03-01 00:00:00

pages

402-10

issue

3

eissn

0145-2126

issn

1873-5835

pii

S0145-2126(13)00453-0

journal_volume

38

pub_type

杂志文章

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