The metastasis inducer CCN1 (CYR61) activates the fatty acid synthase (FASN)-driven lipogenic phenotype in breast cancer cells

Menendez, Javier A.; Vellon, Luciano; Espinoza, Ingrid; Lupu, Ruth

doi:10.18632/oncoscience.314

The metastasis inducer CCN1 (CYR61) activates the fatty acid synthase (FASN)-driven lipogenic phenotype in breast cancer cells

Journal Article · Fri Jul 22 00:00:00 EDT 2016 · Oncoscience

DOI:https://doi.org/10.18632/oncoscience.314· OSTI ID:1629907

Menendez, Javier A. ^[1]; Vellon, Luciano ^[2]; Espinoza, Ingrid ^[3]; Lupu, Ruth ^[4]

Catalan Institute of Oncology, Girona, Catalonia (Spain); Girona Biomedical Research Inst. (IDIBGI), Girona (Spain); DOE/OSTI
CONICET-Laboratorio de Immunohematología, Buenos Aires (Argentina)
University of Mississippi, Jackson, MS (United States)
Mayo Clinic, Rochester, MN (United States); Mayo Clinic Cancer Center, Rochester, MN (United States)

The angiogenic inducer CCN1 (Cysteine-rich 61, CYR61) is differentially activated in metastatic breast carcinomas. However, little is known about the precise mechanisms that underlie the pro-metastatic actions of CCN1. Here, we investigated the impact of CCN1 expression on fatty acid synthase (FASN), a metabolic oncogene thought to provide cancer cells with proliferative and survival advantages. Forced expression of CCN1 in MCF-7 cells robustly up-regulated FASN protein expression and also significantly increased FASN gene promoter activity 2- to 3-fold, whereas deletion of the sterol response element-binding protein (SREBP) binding site in the FASN promoter completely abrogated CCN1-driven transcriptional activation. Pharmacological blockade of MAPK or PI-3’K activation similarly prevented the ability of CCN1 to induce FASN gene activation. Pharmacological inhibition of FASN activity with the mycotoxin cerulenin or the small compound C75 reversed CCN1-induced acquisition of estrogen independence and resistance to hormone therapies such as tamoxifen and fulvestrant in anchorage-independent growth assays. This study uncovers FASN-dependent endogenous lipogenesis as a new mechanism controlling the metastatic phenotype promoted by CCN1. Because estrogen independence and progression to a metastatic phenotype are hallmarks of therapeutic resistance and mortality in breast cancer, this previously unrecognized CCN1-driven lipogenic phenotype represents a novel metabolic target to clinically manage metastatic disease progression.

View Accepted Manuscript (DOE)

Research Organization:: Mayo Clinic, Rochester, MN (United States)

Sponsoring Organization:: Agència de Gestió d’Ajuts Universitaris i de Recerca (AGAUR); Department of Defense (DoD); Ministerio de Ciencia e Innovación; National Institutes of Health (NIH); USDOE Office of Science (SC), Biological and Environmental Research (BER). Biological Systems Science Division

Grant/Contract Number:: AC03-76SF00098; SC0012379

OSTI ID:: 1629907

Journal Information:: Oncoscience, Journal Name: Oncoscience Journal Issue: 7-8 Vol. 3; ISSN 2331-4737

Publisher:: Impact Journals, LLCCopyright Statement

Country of Publication:: United States

Language:: English

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Related Subjects

59 BASIC BIOLOGICAL SCIENCES
CCN1
CYR61
breast cancer
fatty acid synthase
metastasis

The metastasis inducer CCN1 (CYR61) activates the fatty acid synthase (FASN)-driven lipogenic phenotype in breast cancer cells

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