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Histone deacetylase inhibitor, AR‐42, exerts antitumor effects by inducing apoptosis and cell cycle arrest in Y79 cells
Author(s) -
Duan Sujuan,
Gong Xiaona,
Liu Xing,
Cui Wenwen,
Chen Kaddie,
Mao Longbing,
Jun Sun,
Zhou Ruihao,
Sang Yi,
Huang Guofu
Publication year - 2019
Publication title -
journal of cellular physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.529
H-Index - 174
eISSN - 1097-4652
pISSN - 0021-9541
DOI - 10.1002/jcp.28806
Subject(s) - apoptosis , histone deacetylase inhibitor , cell cycle checkpoint , histone deacetylase , chemistry , cell cycle , histone deacetylase 5 , microbiology and biotechnology , cancer research , hdac11 , pharmacology , histone , biology , biochemistry , dna
Retinoblastoma (RB) is the most common type of intraocular malignant tumor that occurs in childhood. AR‐42, a member of a newly discovered class of phenylbutyrate‐derived histone deacetylase inhibitors, exerts antitumor effects on many cancers. In the present study, we initially evaluated the effect of AR‐42 towards RB cells and explored the underlying mechanism in this disease. Our results found that AR‐42 showed powerful antitumor effects at low micromolar concentrations by inhibiting cell viability, blocking cell cycle, stimulating apoptosis in vitro, and suppressing RB growth in a mouse subcutaneous tumor xenograft model. Furthermore, the AKT/nuclear factor‐kappa B signaling pathway was disrupted in Y79 cells treated with AR‐42. In conclusion, we propose that AR‐42 might be a promising drug treatment for RB.