USDA/ARS Children's Nutrition Research Center, Department of Pediatrics, Baylor College of Medicine, Houston, TX, USA.
The Ohio State University Comprehensive Cancer Center, The Ohio State University, Columbus, OH, USA.
J Nutr. 2022 Jun 9;152(6):1381-1403. doi: 10.1093/jn/nxac066.
Human epidemiology suggests a protective effect of tomatoes or tomato phytochemicals, such as lycopene, on prostate cancer risk. However, human epidemiology alone cannot reveal causal relations. Laboratory animal models of prostate cancer provide opportunities to investigate hypotheses regarding dietary components in precisely controlled, experimental systems, contributing to our understanding of diet and cancer risk relations. We review the published studies evaluating the impact of tomatoes and/or lycopene in preclinical models of prostate carcinogenesis and tumorigenesis. The feeding of tomatoes or tomato components demonstrates anti-prostate cancer activity in both transplantable xenograft models of tumorigenesis and models of chemically- and genetically-driven carcinogenesis. Feeding pure lycopene shows anticancer activity in most studies, although outcomes vary by model system, suggesting that the impact of pure lycopene can depend on dose, duration, and specific carcinogenic processes represented in different models. Nonetheless, studies with the transgenic adenocarcinoma of the mouse prostate (TRAMP) model of carcinogenesis typically demonstrate similar bioactivity to that of tomato feeding. In general, interventions that commence earlier in carcinogenesis and are sustained tend to be more efficacious. Accumulated data suggest that lycopene is one, but perhaps not the only, anticancer bioactive compound in tomatoes. Although it is clear that tomatoes and lycopene have anti-prostate cancer activity in rodent models, major knowledge gaps remain in understanding dose-response relations and molecular mechanisms of action. Published and future findings from rodent studies can provide guidance for translational scientists to design and execute informative human clinical trials of prostate cancer prevention or in support of therapy.
人类流行病学表明，番茄或番茄植物化学物质（如番茄红素）对前列腺癌风险具有保护作用。然而，仅靠人类流行病学并不能揭示因果关系。前列腺癌的实验室动物模型为在精确控制的实验系统中研究关于饮食成分的假设提供了机会，有助于我们了解饮食与癌症风险的关系。我们回顾了评估番茄和/或番茄红素对前列腺癌发生和肿瘤发生的临床前模型影响的已发表研究。在肿瘤发生和化学及遗传致癌的移植性异种移植模型中，喂食番茄或番茄成分均显示出抗前列腺癌活性。在大多数研究中，喂食纯番茄红素显示出抗癌活性，尽管结果因模型系统而异，这表明纯番茄红素的影响可能取决于剂量、持续时间和不同模型中代表的特定致癌过程。尽管如此，具有化学致癌作用的转基因鼠前列腺腺癌（TRAMP）模型的研究通常显示出与番茄喂养相似的生物活性。一般来说，起始于更早的致癌阶段并持续进行的干预往往更有效。累积的数据表明，番茄红素是番茄中具有抗癌活性的生物活性化合物之一，但可能不是唯一的一种。尽管番茄和番茄红素在啮齿动物模型中具有抗前列腺癌活性已得到明确证实，但在了解剂量反应关系和作用机制方面仍存在重大知识空白。已发表和未来的啮齿动物研究结果可为转化科学家设计和开展有意义的前列腺癌预防或支持治疗的人类临床试验提供指导。
