Abstract
In this paper we show that acetyltanshinone IIA (ATA), a novel anti-cancer agent, preferentially inhibits cell growth of oestrogen receptor positive (ER+) breast cancer cells and that it is more potent than the commonly used anti-breast cancer agent, tamoxifen. The metabolic product of ATA, hydroquinone tanshinone IIA (HTA) binds to the ERα and causes its degradation mainly in the nucleus via an ubiquitin-mediated proteasome-dependent pathway. In addition, ATA also reduced the mRNA levels of the ERα encoding gene, ESR1, distinguishing ATA from another anti-breast cancer drug, fulvestrant. Finally, ATA reduced the transcription of an ER-responsive gene, GREB1.
Original language | English (US) |
---|---|
Pages (from-to) | 94-103 |
Number of pages | 10 |
Journal | Cancer Letters |
Volume | 346 |
Issue number | 1 |
DOIs | |
State | Published - Apr 28 2014 |
Keywords
- Acetyltanshinone IIA
- Anti-breast cancer agent
- Fulvestrant
- Oestrogen receptor
- Tamoxifen
ASJC Scopus subject areas
- Oncology
- Cancer Research