The actin cytoskeletal architecture of estrogen receptor positive breast cancer cells suppresses invasion
Parker, Sara S.
Adams, Deanna G.
Puleo, Julieann I.
Watson, Adam W.
Hill, Samantha M.
Roe, Denise J.
AffiliationUniv Arizona, BioComp Facil
Univ Arizona, Coll Social & Behav Sci, Sch Geog & Dev
Univ Arizona, Ctr Canc
Univ Arizona, Mel & Enid Zuckerman Coll Publ Hlth
MetadataShow full item record
PublisherNATURE PUBLISHING GROUP
CitationPadilla-Rodriguez, M., Parker, S. S., Adams, D. G., Westerling, T., Puleo, J. I., Watson, A. W., ... Mouneimne, G. (2018). The actin cytoskeletal architecture of estrogen receptor positive breast cancer cells suppresses invasion. Nature Communications, 9(1), . https://doi.org/10.1038/s41467-018-05367-2
Rights© The Author(s) 2018. Open Access This article is licensed under a Creative Commons Attribution 4.0 International License.
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AbstractEstrogen promotes growth of estrogen receptor-positive (ER+) breast tumors. However, epidemiological studies examining the prognostic characteristics of breast cancer in postmenopausal women receiving hormone replacement therapy reveal a significant decrease in tumor dissemination, suggesting that estrogen has potential protective effects against cancer cell invasion. Here, we show that estrogen suppresses invasion of ER+ breast cancer cells by increasing transcription of the Ena/VASP protein, EVL, which promotes the generation of suppressive cortical actin bundles that inhibit motility dynamics, and is crucial for the ERmediated suppression of invasion in vitro and in vivo. Interestingly, despite its benefits in suppressing tumor growth, anti-estrogenic endocrine therapy decreases EVL expression and increases local invasion in patients. Our results highlight the dichotomous effects of estrogen on tumor progression and suggest that, in contrast to its established role in promoting growth of ER+ tumors, estrogen has a significant role in suppressing invasion through actin cytoskeletal remodeling.
VersionFinal published version
SponsorsGordon and Betty Moore Foundation; Howard Hughes Medical Institute; NCI grant [RO1 CA196885-01]; Science Foundation Arizona Bisgrove Scholars Postdoctoral Fellowship; NCI University of Arizona Cancer Center Support Grant [P30CA023074]