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ERα17p, an ERα P 295 ‐T 311 fragment, modifies the migration of breast cancer cells, through actin cytoskeleton rearrangements
Author(s) -
Kampa Marilena,
Pelekanou Vassiliki,
Gallo Dominique,
Notas George,
Troullinaki Maria,
Pediaditakis Iosif,
Charalampopoulos Ioannis,
Jacquot Yves,
Leclercq Guy,
Castanas Elias
Publication year - 2011
Publication title -
journal of cellular biochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.028
H-Index - 165
eISSN - 1097-4644
pISSN - 0730-2312
DOI - 10.1002/jcb.23309
Subject(s) - gper , estrogen receptor , actin cytoskeleton , pi3k/akt/mtor pathway , estrogen receptor alpha , microbiology and biotechnology , cancer cell , cytoplasm , cell migration , biology , cell , cancer research , cytoskeleton , chemistry , signal transduction , cancer , breast cancer , biochemistry , genetics
Recently, our knowledge on estrogen receptor alpha (ERα) functions and fate has progressed: ERα enters in repeated transcription‐modulating cycles (nucleus/cytoplasm/membrane trafficking processes and proteasomal degradation) that are governed by specific protein–protein interactions. Receptor fragments, especially those resulting from the proteolysis of its ligand binding domain, as well as corresponding synthetic peptides, have been studied with respect to their estrogenic/antiestrogenic potency. A peptide, corresponding to the human ERα P 295 ‐T 311 sequence (ERα17p) has been shown to alter breast cancer cell fate, triggering proliferation, or apoptosis. The aim of this work was to explore the effect of ERα17p on breast cancer cell migration and actin cytoskeleton dynamics and further analyze the mechanism of its membrane action. We show that ERα17p increases (MCF‐7 and SK‐BR‐3 cells) or decreases (T47D and MDA‐MB‐231 cells) migration of breast cancer cells, in an ERα‐independent manner, by mechanism(s) depending on Rho/ROCK and PI3K/Akt signaling pathways. Moreover, the peptide enhances the association of both estrogens and androgens to membranes and modifies cell migration, induced by E 2 ‐BSA. Additionally, initial evidence of a possible agonistic action of the peptide on GPR30 is also provided. ERα17p can be considered as a cell migration‐modulator and could therefore constitute a therapeutic challenge, even in anti‐estrogen‐resistant tumors. J. Cell. Biochem. 112: 3786–3796, 2011. © 2011 Wiley Periodicals, Inc.