Journal
JOURNAL OF HEMATOLOGY & ONCOLOGY
Volume 13, Issue 1, Pages -Publisher
BMC
DOI: 10.1186/s13045-020-00949-4
Keywords
Ras; RAF; MEK; ERK signaling; AMPK signaling; Interplay; Tumorigenesis; Cellular metabolism; RAF; MEK; ERK inhibitors; AMPK inhibitors; AMPK activators; Autophagy; Targeted therapy
Categories
Funding
- Asia Fund for Cancer Research [AFCR-2017/2019JH]
- SingHealth Foundation [AM/TP011/2018]
- NMRC [OFIRG18nov-0078]
Ask authors/readers for more resources
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.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available