Division of Oncology, Cincinnati Children's Hospital Medical Center, Cincinnati, Ohio.
Division of Molecular and Developmental Biology, Cincinnati Children's Hospital Medical Center, Cincinnati, Ohio.
Cancer Res. 2024 Jul 15;84(14):2333-2351. doi: 10.1158/0008-5472.CAN-23-1635.
The genetic landscape of cancer cells can lead to specific metabolic dependencies for tumor growth. Dietary interventions represent an attractive strategy to restrict the availability of key nutrients to tumors. In this study, we identified that growth of a subset of melanoma was severely restricted by a rationally designed combination therapy of a stearoyl-CoA desaturase (SCD) inhibitor with an isocaloric low-oleic acid diet. Despite its importance in oncogenesis, SCD underwent monoallelic codeletion along with PTEN on chromosome 10q in approximately 47.5% of melanoma, and the other SCD allele was methylated, resulting in very low-SCD expression. Although this SCD-deficient subset was refractory to SCD inhibitors, the subset of PTEN wild-type melanoma that retained SCD was sensitive. As dietary oleic acid could potentially blunt the effect of SCD inhibitors, a low oleic acid custom diet was combined with an SCD inhibitor. The combination reduced monounsaturated fatty acids and increased saturated fatty acids, inducing robust apoptosis and growth suppression and inhibiting lung metastasis with minimal toxicity in preclinical mouse models of PTEN wild-type melanoma. When combined with anti-PD1 immunotherapy, the SCD inhibitor improved T-cell functionality and further constrained melanoma growth in mice. Collectively, these results suggest that optimizing SCD inhibitors with diets low in oleic acid may offer a viable and efficacious therapeutic approach for improving melanoma treatment. Significance: Blockade of endogenous production of fatty acids essential for melanoma combined with restriction of dietary intake blocks tumor growth and enhances response to immunotherapy, providing a rational drug-diet treatment regimen for melanoma.
癌细胞的遗传特征可能导致肿瘤生长的特定代谢依赖性。饮食干预代表了一种有吸引力的策略,可以限制肿瘤获得关键营养物质的能力。在这项研究中,我们发现,通过合理设计的硬脂酰辅酶 A 去饱和酶(SCD)抑制剂与等热量低油酸饮食联合治疗,可严重限制一部分黑色素瘤的生长。尽管 SCD 在肿瘤发生中很重要,但大约 47.5%的黑色素瘤中 SCD 与 10q 染色体上的 PTEN 发生单等位基因缺失,另一个 SCD 等位基因发生甲基化,导致 SCD 表达非常低。尽管这个 SCD 缺陷亚群对 SCD 抑制剂有抗性,但保留 SCD 的 PTEN 野生型黑色素瘤亚群是敏感的。由于饮食中的油酸可能会削弱 SCD 抑制剂的效果,因此我们将低油酸定制饮食与 SCD 抑制剂联合使用。这种联合治疗减少了单不饱和脂肪酸,增加了饱和脂肪酸,在 PTEN 野生型黑色素瘤的临床前小鼠模型中,诱导了强烈的细胞凋亡和生长抑制,并抑制了肺转移,同时毒性最小。当与抗 PD1 免疫疗法联合使用时,SCD 抑制剂改善了 T 细胞的功能,并进一步限制了小鼠黑色素瘤的生长。总之,这些结果表明,用低油酸饮食优化 SCD 抑制剂可能为改善黑色素瘤治疗提供一种可行且有效的治疗方法。意义:阻断黑色素瘤必需脂肪酸的内源性产生与限制饮食摄入相结合可阻止肿瘤生长并增强对免疫疗法的反应,为黑色素瘤提供了一种合理的药物-饮食治疗方案。