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

作　　者：Salma Abdi Mahmoud Salma Abdi Mahmoud(Department of Obstetrics and Gynaecology, School of Health and Medical Sciences, The State University of Zanzibar, Zanzibar, Tanzania)

机构地区：[1]Department of Obstetrics and Gynaecology, School of Health and Medical Sciences, The State University of Zanzibar, Zanzibar, Tanzania

出　　处：《Open Journal of Obstetrics and Gynecology》2024年第12期1827-1840,共14页妇产科期刊(英文)

摘　　要：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.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.

关 键 词：Intermittent Fasting TUMOR Ras/MAPK PI3K/AKT/MTOR WNT/Β-CATENIN HGF/C-MET 

分 类 号：R73[医药卫生—肿瘤]