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Fascaplysin Sensitizes Anti-Cancer Effects of Drugs Targeting AKT and AMPK

 Taek-In Oh  ;  Jun Ho Lee  ;  Seongman Kim  ;  Taek-Jin Nam  ;  Young-Seon Kim  ;  Byeong Mo Kim  ;  Woo Jong Yim  ;  Ji-Hong Lim 
 MOLECULES, Vol.23(1) : 42, 2018 
Journal Title
Issue Date
Adenylate Kinase/antagonists & inhibitors* ; Adenylate Kinase/metabolism ; Antineoplastic Agents/pharmacology* ; Cell Line, Tumor ; DNA Damage ; Drug Synergism ; Enzyme Activation/drug effects ; Humans ; Indoles/pharmacology* ; Membrane Potential, Mitochondrial/drug effects ; Methotrexate/pharmacology ; Phosphorylation/drug effects ; Protein Kinase Inhibitors/pharmacology* ; Proto-Oncogene Proteins c-akt/antagonists & inhibitors* ; Proto-Oncogene Proteins c-akt/metabolism ; Signal Transduction/drug effects ; Stress, Physiological/drug effects
AKT ; AMPK ; cancer ; chemoresistance ; fascaplysin
Fascaplysin, a natural product isolated from marine sponges, is a potential candidate for the development of anti-cancer drugs. However, the mechanism underlying its therapeutic effect of strengthening anti-cancer efficacy of other drugs is poorly understood. Here, we found that fascaplysin increases phosphorylation of protein kinase B (PKB), also known as AKT, and adenosine monophosphate-activated protein kinase (AMPK), which are considered therapeutic targets for cancer treatment due to their anti-apoptotic or pro-survival functions in cancer. A cell viability assay revealed that pharmacological suppression of AKT using LY294002 enhanced the anti-cancer effect of fascaplysin in various cancer cells. Similarly, fascaplysin was observed to have improved anti-cancer effects in combination with compound C, a selective AMPK inhibitor. Another challenge showed that fascaplysin increased the efficacy of methotrexate (MTX)-mediated cancer therapy by suppressing genes related to folate and purine metabolism. Overall, these results suggest that fascaplysin may be useful for improving the anti-cancer efficacy of targeted anti-cancer drugs, such as inhibitors of phosphoinositide 3-kinase AKT signaling, and chemotherapeutic agents, such as MTX.
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5. Research Institutes (연구소) > Yonsei Integrative Research Institute for Cerebral & Cardiovascular Disease (뇌심혈관질환융합연구사업단) > 1. Journal Papers
Yonsei Authors
Kim, Byeong Mo(김병모) ORCID logo https://orcid.org/0000-0002-0582-3132
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