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Genes (Basel). 2017 Apr 28;8(5). pii: E131. doi: 10.3390/genes8050131.

The Stearoyl-CoA Desaturase-1 (Desat1) in Drosophila cooperated with Myc to Induce Autophagy and Growth, a Potential New Link to Tumor Survival.

Author information

1
Department of Biosciences, University of Milan, Via Celoria 26, 20133 Milan, Italy. chiara.paiardi@unimi.it.
2
Department of Biosciences, University of Milan, Via Celoria 26, 20133 Milan, Italy. zhasmine.mirzoyan@unimi.it.
3
Center of Integrated Biology (CiBio), University of Trento, Via Sommarive 9, 38123 Trento, Italy. sherizola@gmail.com.
4
Crown Bioscience Inc., Santa Clara, CA 950524, USA. fparisi@crownbio.com.
5
Department of Pathology, European Institute of Oncology (IEO), Via Ripamonti 435, 20100 Milan, Italy. andrea.vingiani@unimi.it.
6
Department of Biosciences, University of Milan, Via Celoria 26, 20133 Milan, Italy. maria.pasini@unimi.it.
7
Department of Biosciences, University of Milan, Via Celoria 26, 20133 Milan, Italy. paola.bellosta@unitn.it.
8
Center of Integrated Biology (CiBio), University of Trento, Via Sommarive 9, 38123 Trento, Italy. paola.bellosta@unitn.it.

Abstract

Lipids are an important energy supply in our cells and can be stored or used to produce macromolecules during lipogenesis when cells experience nutrient starvation. Our proteomic analysis reveals that the Drosophila homologue of human Stearoyl-CoA desaturase-1 Desat1) is an indirect target of Myc in fat cells. Stearoyl-CoA desaturases are key enzymes in the synthesis of monounsaturated fatty acids critical for the formation of complex lipids such as triglycerides and phospholipids. Their function is fundamental for cellular physiology, however in tumors, overexpression of SCD-1 and SCD-5 has been found frequently associated with a poor prognosis. Another gene that is often upregulated in tumors is the proto-oncogene c-myc, where its overexpression or increased protein stability, favor cellular growth. Here, we report a potential link between Myc and Desat1 to control autophagy and growth. Using Drosophila, we found that expression of Desat1, in metabolic tissues like the fat body, in the gut and in epithelial cells, is necessary for Myc function to induce autophagy a cell eating mechanism important for energy production. In addition, we observed that reduction of Desat1 affects Myc ability to induce growth in epithelial cells. Our data also identify, in prostatic tumor cells, a significant correlation between the expression of Myc and SCD-1 proteins, suggesting the existence of a potential functional relationship between the activities of these proteins in sustaining tumor progression.

KEYWORDS:

Drosophila; Myc; SCD-1/Desat1; autophagy; growth; lipid metabolism; prostate tumors

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