Our understanding of cancer-specific metabolic changes is currently unclear. In recent years, the fruit fly Drosophila melanogaster with its powerful genetic tools has become an attractive model for studying both tumor autonomous and the systemic processes resulting from the tumor growth. Here we investigated the effect of tumorigenesis on the modulation of lipid droplets (LDs) in the larval fat bodies (mammalian equivalent of adipose tissue). We have overexpressed Notch signaling alone or in combination with the developmental regulator Myocyte enhancer factor 2 (Mef2) using wing-specific and eye-specific drivers, quantified the size of LDs in the fat body of the different tumor bearing larvae, and estimated the expression of genes associated with lipolysis and lipogenesis. We have found that hyperplastic and neoplastic tumor induced by overexpression of Notch and co-expression of Notch and Mef2 respectively triggers impaired lipid metabolism marked by increased size of fat body LDs. The impaired lipid metabolism in tumor carrying larvae is linked to the altered expression of genes that participate in lipolysis and lipogenesis. These findings reveal modulation of LDs as one of the host’s specific response upon tumor initiation. This information could potentially uncover mechanisms for designing innovative approaches to modulate cancer growth.

目前尚不清楚我们对癌症特异性代谢变化的了解。近年来，果蝇果蝇（Drosophila melanogaster）具有强大的遗传工具，已成为研究肿瘤自主性和肿瘤生长导致的系统性过程的有吸引力的模型。在这里，我们研究了肿瘤发生对幼虫脂肪体内（脂肪组织的哺乳动物等效物）脂质滴（LDs）的调节作用。我们已经单独或与发育调节剂心肌细胞增强因子2（Mef2）使用特定于机翼的驱动程序和特定于眼睛的驱动程序，量化了不同荷瘤幼虫脂肪体内LD的大小，并估计了与脂解和脂肪生成相关的基因的表达。我们已经发现，由Notch的过表达以及Notch和Mef2的共表达诱导的增生性和肿瘤性肿瘤分别触发脂代谢受损，其以脂肪体LDs的大小增加为标志。携带肿瘤的幼虫中脂质代谢受损与参与脂肪分解和脂肪形成的基因表达的改变有关。这些发现揭示了LDs的调节是肿瘤发生后宿主特异性反应之一。该信息可能潜在地揭示用于设计创新方法以调节癌症生长的机制。