ArticleCancer biology & medicine2018
Silencing of syndecan-binding protein enhances the inhibitory effect of tamoxifen and increases cellular sensitivity to estrogen.
Article in Cancer biology & medicine, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
3 citing papers in PubMed, 4 citations in OpenAlex.
- Proteoglycans in Breast Cancer: Friends and Foes.Biomolecules · 2025Review
- Proteomic Characterization of Cytoplasmic Lipid Droplets in Human Metastatic Breast Cancer Cells.Frontiers in oncology · 2021Article
- The Value of Monitoring the Behavior of Circulating Tumor Cells at the End of Endocrine Therapy in Breast Cancer Patients.Cancers · 2018Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveTamoxifen 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.
methodsIn 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 pS2 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.
resultsWe 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/ERα ratio in ER-positive BCa tissue samples.
conclusionsSDCBP 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.
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