Chidamide, a histone deacetylase inhibitor, induces growth arrest and apoptosis in multiple myeloma cells in a caspase-dependent manner

Oncology Letters
Xiang-Gui YuanXiao-Ying Zhao


Chidamide, a novel histone deacetylase (HDAC) inhibitor, induces antitumor effects in various types of cancer. The present study aimed to evaluate the cytotoxic effect of chidamide on multiple myeloma and the underlying mechanisms involved. Viability of multiple myeloma cells upon chidamide treatment was determined by the Cell Counting Kit-8 assay. Apoptosis induction and cell cycle alteration were detected by flow cytometry. Specific apoptosis-associated proteins and cell cycle proteins were evaluated by western blot analysis. Chidamide suppressed cell viability in a time- and dose-dependent manner. Chidamide treatment markedly suppressed the expression of type I HDACs and further induced the acetylation of histones H3 and H4. In addition, it promoted G0/G1 arrest by decreasing cyclin D1 and c-myc expression, and increasing phosphorylated-cellular tumor antigen p53 and cyclin-dependent kinase inhibitor 1 (p21) expression in a dose-dependent manner. Treatment with chidamide induced cell apoptosis by upregulating the apoptosis regulator Bax/B-cell lymphoma 2 ratio in a caspase-dependent manner. In addition, the combination of chidamide with bortezomib, a proteasome inhibitor widely used as a therapeutic agent for multiple myelom...Continue Reading


Nov 5, 1997·Experimental Cell Research·M ImotoI B Weinstein
Jan 18, 2003·Blood·Nicholas MitsiadesKenneth C Anderson
Aug 28, 2004·Endocrinology·Maofu FuRichard G Pestell
May 15, 2009·Nature Reviews. Cancer·Tarek Abbas, Anindya Dutta
Jan 12, 2010·Biochemical and Biophysical Research Communications·Lin LiuHong Zhao
Feb 9, 2010·Nature Chemical Biology·James E BradnerRalph Mazitschek
Mar 18, 2011·The New England Journal of Medicine·Antonio Palumbo, Kenneth Anderson
Jul 19, 2011·Journal of Biomedicine & Biotechnology·Claudia P MillerJoya Chandra
Apr 8, 2014·Biochimica Et Biophysica Acta·Gabriel BretonesJavier León
Apr 12, 2014·Biomedicine & Pharmacotherapy = Biomédecine & Pharmacothérapie·You ZhouZhi-Qiang Ning
Apr 29, 2014·Pharmacology & Therapeutics·Prithviraj BoseSteven Grant
Dec 9, 2014·Epigenetics : Official Journal of the DNA Methylation Society·Sridurga MithraprabhuAndrew Spencer
Jan 9, 2016·CA: a Cancer Journal for Clinicians·Rebecca L SiegelAhmedin Jemal
May 18, 2016·Molecular Biology Reports·Sheng-Hao LinJeremy J W Chen
Oct 25, 2016·Biomedicine & Pharmacotherapy = Biomédecine & Pharmacothérapie·Zhaoyun LiuRong Fu
Mar 17, 2017·Journal of Hematology & Oncology·Yuankai ShiYizhuo Zhang
Apr 19, 2017·Biomedicine & Pharmacotherapy = Biomédecine & Pharmacothérapie·Xia LiJie Jin
Jan 10, 2018·CA: a Cancer Journal for Clinicians·Rebecca L SiegelAhmedin Jemal

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Methods Mentioned

histone acetylation
density gradient centrifugation
flow cytometry

Software Mentioned

GraphPad Prism
ModFit LT

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