紫苏醇抗癌活性涉及的代谢和调节途径：体外研究的范围综述

Metabolic and Regulatory Pathways Involved in the Anticancer Activity of Perillyl Alcohol: A Scoping Review of In Vitro Studies.

作者信息

Batista Brochado Ana Carolina, Moraes Júlia Alves de, Rodrigues de Oliveira Bruna, De Souza Lima Victor Hugo, Mariano Eric Domingos, Karande Sachin, Romasco Tea, Leite Paulo Emilio Correa, Mourão Carlos Fernando, Gomes Alves Gutemberg

机构信息

Post-Graduation Program in Science & Biotechnology, Institute of Biology, Fluminense Federal University, Niteroi 24220-900, Brazil.

Clinical Research Unit, Antonio Pedro University Hospital, Fluminense Federal University, Niteroi 24020-140, Brazil.

出版信息

Cancers (Basel). 2024 Nov 29;16(23):4003. doi: 10.3390/cancers16234003.

DOI:10.3390/cancers16234003

PMID:39682189

原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11640718/

Abstract

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.

摘要

背景/目的：紫苏醇（POH）是一种植物来源的化合物，已在多种人类癌症中显示出抗肿瘤活性。了解POH发挥作用的调控途径对于确定新的治疗机会和探索潜在的药物重新定位策略至关重要。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和调控途径。

方法

按照PRISMA-ScR 2018指南，在PubMed、科学网和Scopus数据库中进行了系统检索。

结果

共纳入39项研究，结果显示POH通过调节多种途径发挥其生物学作用，包括调节细胞周期蛋白、细胞周期蛋白依赖性激酶（CDK）和p21，从而影响细胞周期进程。它通过减弱AKT磷酸化、降低聚（ADP-核糖）聚合酶-1（PARP-1）活性、增加半胱天冬酶活性以及FAS受体及其配体FASL来抑制生长并促进细胞死亡。此外，POH可降低细胞外信号调节激酶（ERK）磷酸化、抑制RAS蛋白异戊二烯化并降低钠钾ATP酶活性。