Oestrogen receptor (ER) is expressed in approximately 60%-70% of human breast cancer. Clinical trials and retrospective analyses have shown that ER-positive (ER+) tumours are more tolerant to chemotherapeutic drug resistance than ER-negative (ER−) tumours. In addition, isobavachalcone (IBC) is known as a kind of phytoestrogen with antitumour effect. However, the underlying mechanism of IBC in ER+ breast cancer needs to be elucidated further. Our in vitro experiments showed that IBC could attenuate 17β-estradiol (E2)-induced paclitaxel resistance and that E2 could stimulate CD44 expression in ER+ breast cancer cells but not in ER− cells. Meanwhile, E2 could promote ERα expression to render ER+ breast cancer cells resistant to paclitaxel. Furthermore, we established paclitaxel-resistant breast cancer cell lines and determined the function of ERα in the enhancement of paclitaxel resistance via the regulation of CD44 transcription. IBC down-regulated ERα and CD44 expression and thus inhibited tumour growth in paclitaxel-resistant xenograft models. Overall, our data demonstrated for the first time that IBC could decrease CD44 expression level via the ERα pathway and make ER+ breast cancer cells sensitive to paclitaxel treatment.
|Number of pages||11|
|Journal||Journal of Cellular and Molecular Medicine|
|State||Published - Nov 2018|
Bibliographical noteFunding Information:
the project of Science & Technology of Nanjing, Grant/Award Number: YKK14081; the Natural Science Foundation of Jiangsu Province, Grant/Award Number: BK20150092; the National Natural Science Foundation of China, Grant/Award Number: 81502623; the Key R & D Special Fund of Jiangsu Province, Grant/Award Number: BE2017611
© 2018 The Authors. Journal of Cellular and Molecular Medicine published by John Wiley & Sons Ltd and Foundation for Cellular and Molecular Medicine.
- breast cancer
- oestrogen receptor alpha
- paclitaxel resistance
ASJC Scopus subject areas
- Molecular Medicine
- Cell Biology