Leptin-induced signaling pathways in cancer cell migration and invasion

(2019) Leptin-induced signaling pathways in cancer cell migration and invasion. Cellular Oncology. pp. 243-260. ISSN 2211-3428

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Abstract

BackgroundIncreasing evidence indicates that obesity is associated with tumor development and progression. Leptin is an adipocyte-related hormone with a key role in energy metabolism and whose circulating levels are elevated in obesity. The effect of leptin on cancer progression and metastasis and its underlying mechanisms are still unclear. Leptin can impact various steps in tumor metastasis, including epithelial-mesenchymal transition, cell adhesion to the extracellular matrix (ECM), and proteolysis of ECM components. To do so, leptin binds to its receptor (OB-Rb) to activate signaling pathways and downstream effectors that participate in tumor cell invasion as well as distant metastasis.ConclusionsIn this review, we describe metastasis steps in detail and characterize metastasis-related molecules activated by leptin, which may help to develop a roadmap that guides future work. In addition, we conclude that a profound understanding of the fundamental molecular processes that contribute to leptin-induced metastasis may pave the way for the development of new prognostic molecules and appropriate approaches to the treatment of obesity-related cancers.

Item Type: Article
Keywords: obesity leptin cancer cell migration cell invasion metastasis epithelial-mesenchymal transition large-scale preparation receptor ob-r plasma adiponectin concentrations mechanisms linking obesity focal adhesion kinase breast-cancer matrix metalloproteinases serum leptin clinical-significance
Subjects: QZ Pathology > QZ 200-380 Neoplasms
Divisions: Faculty of Pharmacy and Pharmaceutical Sciences > Department of Clinical Biochemistry
Page Range: pp. 243-260
Journal or Publication Title: Cellular Oncology
Journal Index: ISI
Volume: 42
Number: 3
Identification Number: https://doi.org/10.1007/s13402-019-00428-0
ISSN: 2211-3428
Depositing User: Zahra Otroj
URI: http://eprints.mui.ac.ir/id/eprint/9967

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