Targeting syndecan-1 in breast cancer inhibits osteoclast functions through up-regulation of osteoprotegerin

Journal of Bone Oncology
Peggy Benad-MehnerLorenz C Hofbauer

Abstract

Breast cancer often metastasizes into bone and leads to osteolytic lesions. The underlying mechanisms, however, are complex and not fully understood. Syndecan-1 is a proteoglycan that has various functions relevant for tumor progression including cell-cell communication and cell-matrix interactions. Moreover, its two glycosaminoglycan-binding sites suggest that it may interfere with glycoproteins such as osteoprotegerin, a potent inhibitor of osteoclastogenesis. Thus, we hypothesize that tumor-derived syndecan-1 alters osteoclast biology by modulating osteoprotegerin. Syndecan-1 expression was down-regulated via siRNA and the cell fate of the breast cancer cell lines MCF-7, T-47D, and MDA-MB-231 was investigated. Furthermore, we determined the regulation of syndecan-1 by dexamethasone, a commonly used antiemetic in breast cancer therapy. Additionally, we analyzed the genesis and activity of osteoclasts in indirect co-culture experiments using supernatants from MCF-7 cells with deficient and sufficient levels of syndecan-1. Dexamethasone time- and dose-dependently increased syndecan-1 expression up to 4-fold but did not alter cell behavior. Syndecan-1 up-regulation did not affect the survival or migration of breast cancer cells....Continue Reading

Citations

Jun 24, 2017·Orthodontics & Craniofacial Research·W J RodyL S Holliday

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Methods Mentioned

BETA
FCS
transfection
PCR
Fluorescence
fluorescence microscopy
ELISAs
ELISA

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