Background/Objectives: Perillyl alcohol (POH), a plant-derived compound, has demonstrated anti-tumor activity across various human cancers. Understanding the regulatory pathways through which POH exerts its effects is crucial for identifying new therapeutic opportunities and exploring potential drug repositioning strategies. Therefore, this scoping review aims to provide a comprehensive overview of the metabolic and regulatory pathways involved in the anticancer effects of POH, based on in vitro evidence. Methods: Following the PRISMA-ScR 2018 guidelines, a systematic search was conducted in the PUBMED, Web of Science, and Scopus databases. Results: A total of 39 studies were included, revealing that POH exerts its biological effects by modulating several pathways, including the regulation of cyclins, CDKs, and p21, thereby affecting cell cycle progression. It inhibits growth and promotes cell death by attenuating AKT phosphorylation, reducing PARP-1 activity, increasing caspase activity and the FAS receptor and its ligand FASL. Additionally, POH reduces ERK phosphorylation, inhibits RAS protein isoprenylation, and decreases Na/K-ATPase activity. Conclusions: In conclusion, this review delineates the key regulatory pathways responsible for mediating the biological effects of POH in cancer.
背景/目的：紫苏醇（POH）作为一种植物源性化合物，已在多种人类癌症中显示出抗肿瘤活性。理解POH发挥作用的调控通路对于识别新的治疗机会和探索潜在的药物重定位策略至关重要。因此，本范围综述旨在基于体外证据，全面概述POH抗癌作用所涉及的代谢与调控通路。方法：遵循PRISMA-ScR 2018指南，在PUBMED、Web of Science和Scopus数据库中进行系统检索。结果：共纳入39项研究，结果表明POH通过调控包括周期蛋白、CDK和p21在内的多种通路发挥其生物学效应，从而影响细胞周期进程。它通过减弱AKT磷酸化、降低PARP-1活性、增加caspase活性以及FAS受体及其配体FASL的表达，来抑制生长并促进细胞死亡。此外，POH还能降低ERK磷酸化、抑制RAS蛋白异戊二烯化并减少Na/K-ATP酶活性。结论：综上所述，本综述阐明了介导POH在癌症中生物学效应的关键调控通路。
肿瘤(癌症)患者之家