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Estrogen receptors as regulators of syndecan‐4 expression in solid tumors
Author(s) -
Karamanos Nikos K,
Gialeli Chrisostomi,
Tsonis Anastasios
Publication year - 2010
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.24.1_supplement.lb104
Subject(s) - estrogen receptor , cancer research , receptor , signal transduction , epidermal growth factor receptor , epidermal growth factor , crosstalk , biology , estrogen receptor alpha , tyrosine kinase , receptor tyrosine kinase , estrogen , endocrinology , growth factor receptor , medicine , microbiology and biotechnology , chemistry , breast cancer , cancer , physics , optics
Estrogens regulate several physiological processes and are implicated in the growth of solid tumors, such as breast and colon. 17â‐estradiol (E2), particularly influences estrogen receptor (ER) expression. ER is synthesized in many cell types as two protein forms, ERá and ERâ, which are products of separate genes. E2 signaling is supposed to be mediated via linear pathway involving insulin‐like growth factor receptor (IGF‐R) and epidermal growth factor receptor (EGFR). The aim of this study was therefore to examine whether estradiol affects the expression of ERs and proteoglycans (PGs) implicated in breast and colon cancers as well as whether this effect is associated with ER/IGF‐R/EGFR system. In vitro studies were performed on a panel of breast and colon cell lines in the presence or absence of E2 and specific IGF‐R, EGFR tyrosine kinase inhibitors. The results showed that E2 affected on the gene expression of syndecan‐4 and is closely related with the expression balance between ERá/ERâ and the crosstalk between crucial ER/IGF‐R/EGFR pathways.