Roles of PPAR activation in cancer therapeutic resistance: Implications for combination therapy and drug development

癌症 过氧化物酶体增殖物激活受体 癌症干细胞 癌细胞 癌症研究 抗药性 生物 药理学 医学 受体 内科学 微生物学
作者
Yanxia Zhang,Bin Xiao,Yunduo Liu,Shunhong Wu,Xiang Qin,Yuhan Xiao,Junxiu Zhao,Ruanfei Yuan,Keping Xie,Linhai Li
出处
期刊:European Journal of Pharmacology [Elsevier BV]
卷期号:964: 176304-176304 被引量:7
标识
DOI:10.1016/j.ejphar.2023.176304
摘要

Therapeutic resistance is a major obstacle to successful treatment or effective containment of cancer. Peroxisome proliferator-activated receptors (PPARs) play an essential role in regulating energy homeostasis and determining cell fate. Despite of the pleiotropic roles of PPARs in cancer, numerous studies have suggested their intricate relationship with therapeutic resistance in cancer. In this review, we provided an overview of the roles of excessively activated PPARs in promoting resistance to modern anti-cancer treatments, including chemotherapy, radiotherapy, targeted therapy, and immunotherapy. The mechanisms through which activated PPARs contribute to therapeutic resistance in most cases include metabolic reprogramming, anti-oxidant defense, anti-apoptosis signaling, proliferation-promoting pathways, and induction of an immunosuppressive tumor microenvironment. In addition, we discussed the mechanisms through which activated PPARs lead to multidrug resistance in cancer, including drug efflux, epithelial-to-mesenchymal transition, and acquisition and maintenance of the cancer stem cell phenotype. Preliminary studies investigating the effect of combination therapies with PPAR antagonists have suggested the potential of these antagonists in reversing resistance and facilitating sustained cancer management. These findings will provide a valuable reference for further research on and clinical translation of PPAR-targeting treatment strategies.
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