Modulation of Estrogen α and Progesterone Receptors in Triple Negative Breast Cancer Cell Lines: The Effects of Vorinostat and Indole-3-Carbinol In Vitro

被引:17
|
作者
Nouriemamzaden, Fatemeh [1 ]
Word, Beverly [1 ]
Cotton, Ebony [1 ]
Hawkins, Anfernee [1 ]
Littlejohn, Kai [1 ]
Moore, Rhonda [2 ]
Miranda-Carbon, Gustav [3 ]
Orish, Chinna Nneka [4 ]
Lyn-Cook, Beverly [1 ]
机构
[1] US FDA, Div Biochem Toxicol, NCTR, HFT 100, Jefferson, AR 72079 USA
[2] US FDA, Div Nonprescript Drugs, Ctr Drug Evaluat Res, White Oak, MD USA
[3] Univ Tennessee, Ctr Hlth Sci, Div Hematol Oncol, Memphis, TN 38163 USA
[4] Univ Port Harcourt, Fac Basic Med Sci, Dept Anat, Port Harcourt, Nigeria
关键词
Vorinostat; I3C; triple negative breast cancer; estrogen receptor; progesterone receptor; HDAC activity; HDAC7; HISTONE DEACETYLASE INHIBITORS; RISK; WOMEN; PROLIFERATION; COMBINATION; APOPTOSIS; INVASION; ACETYLATION; ASSOCIATION; EPIGENETICS;
D O I
10.21873/anticanres.14356
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
Background/Aim: Triple negative cancer (TNBC) is a subtype of breast cancer that is highly aggressive, with poor prognosis and responds differently to treatments. This study investigated the role of vorinostat and indole-3-carbinol (I3C) on regulating critical receptors that are not normally expressed in TNBC. Materials and Methods: Using real-time PCR, immunostaining, and western blots, the re-expression of estrogen receptor alpha (ER), progesterone receptor (PR) and human epidermal growth factor receptor-2 (HER2) receptors was examined in four different TNBC cell types. Results: ER alpha was re-expressed in three subtypes using vorinostat and I3C. Re-expression of the PR by vorinostat was also detected. Neither vorinostat nor I3C resulted in re-expression of the HER2 receptor. A significant decrease in growth and sensitivity to tamoxifen was also noted. Conclusion: The results of this study show that vorinostat and I3C modulate the re-expression of critical receptors in certain subtypes of TNBC through several pathways and these effects can be influenced by the molecular profiles of TNBCs.
引用
收藏
页码:3669 / 3683
页数:15
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