Open AccessTrichostatin A inhibits proliferation of triple negative breast cancer cells by inducing cell cycle arrest and apoptosis
Author(s) -
Xiaowei Song,
Jicang Wu,
Xiangning Yu,
Xiaochun Yang,
Yue Yang
Publication year - 2018
Publication title -
neoplasma
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.628
H-Index - 50
eISSN - 1338-4317
pISSN - 0028-2685
DOI - 10.4149/neo_2018_181212n476
Subject(s) - triple negative breast cancer , trichostatin a , cancer research , breast cancer , apoptosis , cyclin dependent kinase 6 , cyclin d1 , cell growth , cell cycle , cell cycle checkpoint , carcinogenesis , cancer , medicine , biology , histone deacetylase , histone , biochemistry , genetics , gene
Triple negative breast cancer (TNBC) is the most aggressive subtype of breast cancer with poor outcome. Because of lacking therapeutic targets, chemotherapy is the main treatment option for patients with TNBC. Overexpression of HDACs correlates with tumorigenesis, highlighting the potential of HDACs as therapeutic targets for TNBC. Here we demonstrate that trichostatin A (TSA, a HDAC inhibitor) selectively inhibits the proliferation of TNBC cell lines HCC1806 and HCC38 rather than a normal breast cell line MCF10A. The inhibition of TNBC by TSA is via its roles in inducing cell cycle arrest and apoptosis. TSA treatment leads to decreased expression of CYCLIN D1, CDK4, CDK6 and BCL-XL, but increased P21 expression. Moreover, combination of TSA with doxorubicin has synergistic effects on inhibiting proliferation of HCC1806 and HCC38 cells. Our studies identified a promising epigenetic-based therapeutic strategy that may be implemented in the therapy of fatal human breast cancer.