The potential role of targeting the leptin receptor as a treatment for breast cancer in the context of hyperleptinemia: a literature review.
Autor: | Neamah AS; Department of Biology, College of Sciences, University of Baghdad, Baghdad, Iraq. Abbas.Saad2102@sc.uobaghdad.edu.iq., Wadan AS; Oral Biology Department, Faculty of Dentistry, Galala University, Galala Plateau, Attaka, Suez Governorate, 15888, Egypt., Lafta FM; Department of Biology, College of Sciences, University of Baghdad, Baghdad, Iraq., Elakwa DE; Department of Biochemistry & Molecular Biology, Faculty of Pharmacy for Girls, Al-Azhar University, Cairo, Egypt.; Department of Biochemistry, Faculty of Pharmacy, Sinai University, Kantra Branch, Ismailia, Egypt. |
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Jazyk: | angličtina |
Zdroj: | Naunyn-Schmiedeberg's archives of pharmacology [Naunyn Schmiedebergs Arch Pharmacol] 2024 Nov 20. Date of Electronic Publication: 2024 Nov 20. |
DOI: | 10.1007/s00210-024-03592-9 |
Abstrakt: | Since cancer is becoming a leading cause of death worldwide, efforts should be concentrated on understanding its underlying biological alterations that would be utilized in disease management, especially prevention strategies. Within this context, multiple bodies of evidence have highlighted leptin's practical and promising role, a peptide hormone extracted from adipose and fatty tissues with other adipokines, in promoting the proliferation, migration, and metastatic invasion of breast carcinoma cells. Excessive blood leptin levels and hyperleptinemia increase body fat content and stimulate appetite. Also, high leptin level is believed to be associated with several conditions, including overeating, emotional stress, inflammation, obesity, and gestational diabetes. It has been noted that when leptin has impaired signaling in CNS, causing the lack of its normal function in energy balance, it results in leptin resistance, leading to a rise in its concentration in peripheral tissues. Our research paper will shed highlighting on potentially targeting the leptin receptor and its cellular signaling in suppressing breast cancer progression. Competing Interests: Declarations. Ethics approval: Not applicable. Competing interests: The authors declare no competing interests. (© 2024. The Author(s), under exclusive licence to Springer-Verlag GmbH Germany, part of Springer Nature.) |
Databáze: | MEDLINE |
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