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The MAPK and AMPK signalings: interplay and implication in targeted cancer therapy
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Journal Article
The MAPK and AMPK signalings: interplay and implication in targeted cancer therapy
2020
Overview
Cancer is characterized as a complex disease caused by coordinated alterations of multiple signaling pathways. The Ras/RAF/MEK/ERK (MAPK) signaling is one of the best-defined pathways in cancer biology, and its hyperactivation is responsible for over 40% human cancer cases. To drive carcinogenesis, this signaling promotes cellular overgrowth by turning on proliferative genes, and simultaneously enables cells to overcome metabolic stress by inhibiting AMPK signaling, a key singular node of cellular metabolism. Recent studies have shown that AMPK signaling can also reversibly regulate hyperactive MAPK signaling in cancer cells by phosphorylating its key components, RAF/KSR family kinases, which affects not only carcinogenesis but also the outcomes of targeted cancer therapies against the MAPK signaling. In this review, we will summarize the current proceedings of how MAPK-AMPK signalings interplay with each other in cancer biology, as well as its implications in clinic cancer treatment with MAPK inhibition and AMPK modulators, and discuss the exploitation of combinatory therapies targeting both MAPK and AMPK as a novel therapeutic intervention.
Publisher
BioMed Central,BioMed Central Ltd,Springer Nature B.V,BMC
Subject
/ Antineoplastic Agents - therapeutic use
/ Biology
/ Cancer
/ Cell Differentiation - physiology
/ Extracellular signal-regulated kinase
/ Humans
/ Kinases
/ MAP Kinase Signaling System - drug effects
/ MAP Kinase Signaling System - physiology
/ Medicine
/ Mutation
/ Neoplasm Proteins - antagonists & inhibitors
/ Neoplasm Proteins - physiology
/ Oncology
/ Protein Kinase Inhibitors - therapeutic use
/ Protein Processing, Post-Translational
/ Proteins
/ Proto-Oncogene Proteins p21(ras) - antagonists & inhibitors
/ Proto-Oncogene Proteins p21(ras) - genetics
/ Proto-Oncogene Proteins p21(ras) - physiology
/ raf Kinases - antagonists & inhibitors
/ Review
/ Sulindac
