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Christensen, J.G., Schreck, R., Burrows, J., Kuruganti, P., Chan, E., Le, P., et al. (2003) A Selective Small Molecule Inhibitor of c-Met Kinase Inhibits c-Met-Dependent Phenotypes in Vitro and Exhibits Cytoreductive Antitumor Activity in Vivo. Cancer Research, 63, 7345-7355.

has been cited by the following article:

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

  AUTHORS: Salma Abdi Mahmoud

  KEYWORDS: Intermittent Fasting, Tumor, Ras/MAPK, PI3K/AKT/mTOR, Wnt/β-Catenin, HGF/c-Met

  JOURNAL NAME: Open Journal of Obstetrics and Gynecology, Vol.14 No.12, December 19, 2024

  ABSTRACT: Several 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 factor/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.