
Tamoxifen promotes apoptosis and inhibits invasion in estrogen-positive breast cancer MCF-7 cells
Author(s) -
Wei Li,
Xuhua Shi,
Yan Xu,
Jian Wan,
Shaohua Wei,
Ran Zhu
Publication year - 2017
Publication title -
molecular medicine reports
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.727
H-Index - 56
eISSN - 1791-3004
pISSN - 1791-2997
DOI - 10.3892/mmr.2017.6603
Subject(s) - mcf 7 , tamoxifen , antiestrogen , apoptosis , cancer research , breast cancer , cancer cell , oncogene , estrogen , cancer , reactive oxygen species , cell growth , cell , estrogen receptor , biology , cell cycle , medicine , endocrinology , microbiology and biotechnology , human breast , biochemistry
Tamoxifen (TAM) is the earliest non-steroidal antiestrogen drug, which has been widely used in endocrine therapy targeting breast cancer. The aim of the present study was to investigate the effect of TAM on the proliferation, apoptosis, migration and invasion of the estrogen‑positive (ER+) breast cancer cell line MCF‑7 in vitro, and elucidate its mechanisms. It was demonstrated that TAM suppressed proliferation, migration and invasion, and induced apoptosis in MCF‑7 cells. Further investigation revealed that the mitochondrial membrane potential and the amount of ATP were significantly decreased following the treatment of MCF‑7 cells with TAM. Mitochondria are an important source of reactive oxygen species (ROS) and they are also the target of ROS as well. In the present study, TAM promoted the formation of ROS in MCF‑7 cells. In conclusion, these results reveal the underlying mechanism by which TAM induces ER+ breast cancer cell apoptosis and inhibits invasion, thereby supporting the use of TAM in breast cancer treatment.