Increased High Molecular Weight FGF2 in Endocrine-Resistant Breast Cancer View Full Text


Ontology type: schema:ScholarlyArticle     


Article Info

DATE

2018-10

AUTHORS

Ana Sahores, Virginia Figueroa, María May, Marcos Liguori, Adrián Rubstein, Cynthia Fuentes, Britta M. Jacobsen, Andrés Elía, Paola Rojas, Gonzalo R. Sequeira, Michelle M. Álvarez, Pedro González, Hugo Gass, Stephen Hewitt, Alfredo Molinolo, Claudia Lanari, Caroline A. Lamb

ABSTRACT

Endocrine resistance may develop as a consequence of enhanced growth factor signaling. Fibroblast growth factor 2 (FGF2) consists of a low and several high molecular weight forms (HMW-FGF2). We previously demonstrated that antiprogestin-resistant mammary carcinomas display lower levels of progesterone receptor A isoforms (PRA) than B isoforms (PRB). Our aim was to evaluate the role of FGF2 isoforms in breast cancer progression. We evaluated FGF2 expression, cell proliferation, and pathway activation in models with different PRA/PRB ratios. We performed lentiviral infections of different FGF2 isoforms using the human hormone-responsive T47D-YA cells, engineered to only express PRA, and evaluated tumor growth, metastatic dissemination, and endocrine responsiveness. We assessed FGF2 expression and localization in 81 human breast cancer samples. Antiprogestin-resistant experimental mammary carcinomas with low PRA/PRB ratios and T47D-YB cells, which only express PRB, displayed higher levels of HMW-FGF2 than responsive variants. HMW-FGF2 overexpression in T47D-YA cells induced increased tumor growth, lung metastasis, and antiprogestin resistance compared to control tumors. In human breast carcinomas categorized by their PRA/PRB ratio, we found nuclear FGF2 expression in 55.6% of tumor cells. No differences were found between nuclear FGF2 expression and Ki67 proliferation index, tumor stage, or tumor grade. In low-grade tumor samples, moderate to high nuclear FGF2 levels were associated to carcinomas with low PRA/PRB ratio. In conclusion, we show that HMW-FGF2 isoforms are PRB targets which confer endocrine resistance and are localized in the nuclei of breast cancer samples. Hence, targeting intracellular FGF2 may contribute to overcome tumor progression. More... »

PAGES

338-348

Identifiers

URI

http://scigraph.springernature.com/pub.10.1007/s12672-018-0339-4

DOI

http://dx.doi.org/10.1007/s12672-018-0339-4

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1105199844

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/29956066


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