Leptin Signaling in Breast Cancer and Its Crosstalk With Peroxisome Proliferator-Activated Receptors Α and Γ Publisher Pubmed

Summary: A review suggests obesity hormone leptin and PPARs may drive breast cancer, offering clues for new treatments. #CancerResearch #BreastCancer

Dana N¹ ; Ferns GA² ; Nedaeinia R³ ; Haghjooy Javanmard S¹
Source: Clinical and Translational Oncology Published:2023

Abstract

Obesity may create a mitogenic microenvironment that influences tumor initiation and progression. The obesity-associated adipokine, leptin regulates energy metabolism and has been implicated in cancer development. It has been shown that some cell types other than adipocytes can express leptin and leptin receptors in tumor microenvironments. It has been shown that peroxisome proliferator-activated receptors (PPAR) agonists can affect leptin levels and vice versa leptin can affect PPARs. Activation of PPARs affects the expression of several genes involved in aspects of lipid metabolism. In addition, PPARs regulate cancer cell progression through their action on the tumor cell proliferation, metabolism, and cellular environment. Some studies have shown an association between obesity and several types of cancer, including breast cancer. There is some evidence that suggests that there is crosstalk between PPARs and leptin during the development of breast cancer. Through a systematic review of previous studies, we have reviewed the published relevant articles regarding leptin signaling in breast cancer and its crosstalk with peroxisome proliferator-activated receptors α and γ. © 2022, The Author(s), under exclusive licence to Federacion de Sociedades Espanolas de Oncologia (FESEO).