Intermittent Fasting (IF) Reduces Tumor Metastasis via Ras/MAPK, PI3K/AKT/mTOR, Wnt/β-Catenin, and HGF/c-Met Pathways

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dc.contributor.authorMAHMOUD, Salma Abdi
dc.date.accessioned2025-01-02T08:17:30Z
dc.date.available2025-01-02T08:17:30Z
dc.date.issued2024-12-19
dc.descriptionIn this review, we discuss the regulatory mechanism of IF in tumor metastasis by downregulating key OS pathways such as Ras/Raf/MAPK, PI3K/AKT/mTOR, Wnt/β-catenin, and HGF/c-Met.
dc.description.abstractSeveral recent scientific interventions have been conducted to investigate the effects of intermittent fasting (IF) on tumor metastasis. It is well known that IF has a positive effect on reducing OS in the human body. OS is an important factor that leads to DNA damage and stimulates carcinogenesis through dysregulation of signaling pathways that are important for tumor survival and metastasis. Studies have demonstrated that mitogen-activated protein kinase (Ras/MAPK), phosphatidylinositol- 3-kinase/mammalian target of rapamycin (PI3K/AKT/mTOR), Wnt Beta Catenin (Wnt/β-catenin), and hepatocyte growth actor/mesenchymal- epithelial transition factor (HGF/c-Met) are activated in response to the overproduction of OS and may result in carcinogenesis and tumor metastasis. In this review, we discuss the regulatory mechanism of IF in tumor metastasis by downregulating key OS pathways such as Ras/Raf/MAPK, PI3K/AKT/mTOR, Wnt/β-catenin, and HGF/c-Met.
dc.identifier.citationMahmoud, S.A. (2024) Intermittent Fasting (IF) Reduces Tumor Metastasis via Ras/MAPK, PI3K/AKT/mTOR, Wnt/β-Catenin, and HGF/c-Met Pathways. Open Journal of Obstetrics and Gynecology, 14, 1827-1840. https://doi.org/10.4236/ojog.2024.1412152
dc.identifier.issn2160-8806
dc.identifier.urihttps://repository.suza.ac.tz/handle/123456789/327
dc.language.isoen
dc.publisherOpen Journal of Obstetrics and Gynecology / Scientific Reseach Publishing
dc.relation.ispartofseries2024, 14, 1827-1840
dc.titleIntermittent Fasting (IF) Reduces Tumor Metastasis via Ras/MAPK, PI3K/AKT/mTOR, Wnt/β-Catenin, and HGF/c-Met Pathways
dc.typeArticle
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