Journal Article

The SDF-1α/CXCR4 axis induces the expression of fatty acid synthase via sterol regulatory element-binding protein-1 activation in cancer cells

KyeongJin Kim, Hye Young Kim, Hyun Kook Cho, Ki Hyeong Kim and JaeHun Cheong

in Carcinogenesis

Volume 31, issue 4, pages 679-686
Published in print April 2010 | ISSN: 0143-3334
Published online January 2010 | e-ISSN: 1460-2180 | DOI: http://dx.doi.org/10.1093/carcin/bgp329
The SDF-1α/CXCR4 axis induces the expression of fatty acid synthase via sterol regulatory element-binding protein-1 activation in cancer cells

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Fatty acid synthase (FASN), a key enzyme that synthesizes long-chain fatty acids, is involved in both normal lipid synthesis and cancer development. Overexpression and increased activity of FASN represents one of the most frequent phenotypic alterations in cancer cells. Multiple growth factors and growth factor receptors have emerged as major contributors to FASN overexpression. However, the ultimate mechanisms responsible for tumor-associated FASN overexpression are not completely understood. Here, we show that the stromal cell-derived factor-1 alpha (SDF-1α)/CXCR4 axis can induce the FASN expression via the nuclear translocation of sterol regulatory element-binding protein-1, a major modulator of FASN transcription. We also identified that recombinant SDF-1α-induced phosphatidylinositol-3′-kinase/protein kinase B (Akt) phosphorylation was involved in the expression or activities of FASN. Finally, we demonstrated that FASN inhibition significantly reduced the SDF-1α-mediated G1 cyclin expression and cell viability. Taken together, our findings manifest that the SDF-1α/CXCR4 axis is a novel upstream pathway of FASN expression and is associated with mediating its prosurvival effect.

Journal Article.  5319 words.  Illustrated.

Subjects: Clinical Cytogenetics and Molecular Genetics

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