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ACT001 can prevent and reverse tamoxifen resistance in human breast cancer cell lines by inhibiting NF‐κB activation
Author(s) -
Jin XiaoHan,
Jia YongSheng,
Shi YeHui,
Li QiuYing,
Bao ShiQi,
Lu WenPing,
Tong ZhongSheng
Publication year - 2019
Publication title -
journal of cellular biochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.028
H-Index - 165
eISSN - 1097-4644
pISSN - 0730-2312
DOI - 10.1002/jcb.27146
Subject(s) - tamoxifen , cancer research , breast cancer , apoptosis , estrogen receptor , nf κb , medicine , signal transduction , transcription factor , cancer , biology , pharmacology , oncology , endocrinology , gene , microbiology and biotechnology , biochemistry
Endocrine therapy is one of the main treatments for estrogen receptor–positive breast cancers. Tamoxifen is the most commonly used drug for endocrine therapy. However, primary or acquired tamoxifen resistance occurs in a large proportion of breast cancer patients, leading to therapeutic failure. We found that the combination of tamoxifen and ACT001, a nuclear factor‐κB (NF‐κB) signaling pathway inhibitor, effectively inhibited the proliferation of both tamoxifen‐sensitive and tamoxifen‐resistant cells. The tamoxifen‐resistant cell line MCF7R/LCC9 showed active NF‐κB signaling and high apoptosis‐related gene transcription, especially for antiapoptotic genes, which could be diminished by treatment with ACT001. These results demonstrate that ACT001 can prevent and reverse tamoxifen resistance by inhibiting NF‐κB activation.