Open AccessChidamide acts on the histone deacetylase‐mediated miR ‐34a/Bcl‐2 axis to regulate NB4 cell line proliferation and apoptosis
Author(s) -
Peng Jie,
Li ShuJun,
Fu Xiao,
Liu Yi,
Zhao XieLan
Publication year - 2020
Publication title -
the kaohsiung journal of medical sciences
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.439
H-Index - 36
eISSN - 2410-8650
pISSN - 1607-551X
DOI - 10.1002/kjm2.12283
Subject(s) - acute promyelocytic leukemia , cancer research , histone deacetylase , apoptosis , cell growth , retinoic acid , leukemia , cell culture , medicine , histone deacetylase inhibitor , microbiology and biotechnology , biology , histone , biochemistry , immunology , genetics , gene
Acute promyelocytic leukemia (APL), a biologically and clinically distinct variant of acute myelogenous leukemia, is characterized by the fusion of the N‐terminus of promyelocytic leukemia protein to the C terminus of retinoic acid receptor alpha, mostly due to chromosomal translocation t(15;17). Chidamide, a synthetic analogue of MS‐275 identified from a group of benzamide‐type compounds, has been found to have efficient anticancer activity in basic and clinical research studies. However, the concrete role and underlying mechanism of Chidamide in the treatment of APL has not been well characterized. Our data demonstrate that Chidamide inhibited the expression of histone deacetylase (HDAC) to induce apoptosis and suppress proliferation in NB4 cells. Mechanistically, Chidamide increases the expression of miR‐34a by suppressing HDAC. Furthermore, B‐cell lymphoma‐2 (Bcl‐2) is a direct target of miR‐34a, the expression of which is regulated by miR‐34a. Functionally, Chidamide inhibits cell proliferation and promotes apoptosis through miR‐34a/Bcl‐2. Chidamide exerts its anticancer effect via the HDAC‐mediated miR‐34a/Bcl‐2 axis, providing potential targets for APL therapy.