Objective:Tamoxifen is used as a complementary treatment for estrogen receptor(ER)-positive breast cancer(BCa),but many patients developed resistance.The aim of this study was to examine the role of syndecan-binding p...Objective:Tamoxifen is used as a complementary treatment for estrogen receptor(ER)-positive breast cancer(BCa),but many patients developed resistance.The aim of this study was to examine the role of syndecan-binding protein(SDCBP)silencing in ER-positive BCa cells.Methods:In MCF-7/T47D cells,the effects of SDCBP silence/overexpression on cell proliferation and estrogenic response were examined.Cell proliferation was examined using the MTT assay and cell cycle regulators were examined by Western blot.Estrogen response was examined from a luciferase activity and evaluation of transcript levels of p S2 and progesterone receptor(PR)upon estrogen administration.Samples of ER-positive BCa were stained with ERα,PR,and SDCBP antibodies,and their expression correlations were analyzed.Results:We found that SDCBP silencing inhibited the proliferation of ER-positive BCa cells and arrested a greater number of cells in the G1 phase of the cell cycle compared to tamoxifen alone,while SDCBP overexpression limited the anti-cancer effects of tamoxifen.SDCBP silencing and overexpression also enhanced and attenuated the estrogenic response,respectively.Expression of SDCBP was negatively correlated with PR,ERα,and the PR/ERαratio in ER-positive BCa tissue samples.Conclusions:SDCBP may be involved in tamoxifen resistance in ER-positive BCa.Tamoxifen treatment combined with SDCBP silencing may provide a novel treatment for endocrine therapy-resistant BCa.展开更多
基金supported by National Natural Science Foundation of China (Grant No. 81302292 to Xiaolong Qian, Grant No. 81702629 to Jun Zhang, Grant No. 81672636 and 81272358 to Feng Gu, Grant No. 81672637 to Li Fu)
文摘Objective:Tamoxifen is used as a complementary treatment for estrogen receptor(ER)-positive breast cancer(BCa),but many patients developed resistance.The aim of this study was to examine the role of syndecan-binding protein(SDCBP)silencing in ER-positive BCa cells.Methods:In MCF-7/T47D cells,the effects of SDCBP silence/overexpression on cell proliferation and estrogenic response were examined.Cell proliferation was examined using the MTT assay and cell cycle regulators were examined by Western blot.Estrogen response was examined from a luciferase activity and evaluation of transcript levels of p S2 and progesterone receptor(PR)upon estrogen administration.Samples of ER-positive BCa were stained with ERα,PR,and SDCBP antibodies,and their expression correlations were analyzed.Results:We found that SDCBP silencing inhibited the proliferation of ER-positive BCa cells and arrested a greater number of cells in the G1 phase of the cell cycle compared to tamoxifen alone,while SDCBP overexpression limited the anti-cancer effects of tamoxifen.SDCBP silencing and overexpression also enhanced and attenuated the estrogenic response,respectively.Expression of SDCBP was negatively correlated with PR,ERα,and the PR/ERαratio in ER-positive BCa tissue samples.Conclusions:SDCBP may be involved in tamoxifen resistance in ER-positive BCa.Tamoxifen treatment combined with SDCBP silencing may provide a novel treatment for endocrine therapy-resistant BCa.
