Abstract
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.
Highlights
Breast cancer is one of the most common malignant tumours in women, with high rate of morbidity and metastasis.[1]
To further explore whether CD44 expression was regulated by equally.receptor alpha (ERa), we examined the expression of CD44 in ZR-75-1 and MCF-7 cells transfected with ERa
In this study, using our established paclitaxel-resistant breast cancer cells, we explored whether and how IBC influenced paclitaxel resistance in breast cancer cells via the ERa-dependent pathway
Summary
Breast cancer is one of the most common malignant tumours in women, with high rate of morbidity and metastasis.[1]. Receptor alpha (ERa) is positive in approximately 60%-70% of breast cancer patients.[2,3] Cumulative data show that ERa+ breast cancer cells are more resistant to paclitaxel, a first-line chemotherapeutic drug for breast cancer, than are ER- breast cancer.[4,5] chemotherapy failure caused by paclitaxel resistance is considered a substantial obstacle in the treatment of ER+ breast cancer.[6,7] For the first time, our results demonstrated that inhibition of ERa by IBC can down-regulate CD44 expression and decrease paclitaxel resistance in ER+ breast cancer cells and xenograft tumour models
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