RRC ID 38551
Author Yang D, Yaguchi T, Nakano T, Nishizaki T.
Title Adenosine activates AMPK to phosphorylate Bcl-XL responsible for mitochondrial damage and DIABLO release in HuH-7 cells.
Journal Cell Physiol Biochem
Abstract BACKGROUND/AIMS:Accumulating evidence has pointed to AMP-activated protein kinase (AMPK) as an inducer of apoptosis in a variety of cancer cells. The present study aimed at understanding AMPK signals for adenosine-induced HuH-7 cell apoptosis.
METHODS:Cell viability, AMPK activity, mitochondrial membrane potentials, phosphorylation of Bcl-X(L), in situ DIABLO mobilizations, and caspase-3 activity were monitored in HuH-7 cells. Plasmid DNAs for DIABLO-GFP, mutant Bcl-X(L), dominant negative mutant AMPKα2 and the siRNAs to silence the AMPKα1 or AMPKα2 targeted gene were constructed and transfected.
RESULTS:Adenosine or the AMPK activator AICAR induced apoptosis in HuH-7 cells, and no synergistic effect was obtained with co-treatment. Adenosine activated AMPK, to phosphorylate Bcl-X(L). Adenosine or AICAR disrupted mitochondrial membrane potentials, and the effect was inhibited by knocking-down AMPKα1 and/or AMPKα2, expressing dominant negative mutant AMPKα2 or mutant Bcl-X(L) lacking Ser/Thr phosphorylation sites. AICAR stimulated DIABLO release from the mitochondria, and the release was suppressed by expressing the mutant Bcl-X(L). AICAR activated caspase-3, which was also inhibited by expressing the mutant Bcl-X(L).
CONCLUSION:Adenosine activates AMPK, to disrupt mitochondrial membrane potentials through Bcl-X(L) phosphorylation, allowing DIABLO release from the mitochondria, as a factor for caspase-3 activation to induce HuH-7 cell apoptosis.
Volume 27(1)
Pages 71-8
Published 2011-1-1
DOI 10.1159/000325207
PII 000325207
PMID 21325824
MeSH AMP-Activated Protein Kinases / genetics AMP-Activated Protein Kinases / metabolism* Adenosine / pharmacology* Aminoimidazole Carboxamide / analogs & derivatives Aminoimidazole Carboxamide / pharmacology Apoptosis Apoptosis Regulatory Proteins Cell Line, Tumor Humans Intracellular Signaling Peptides and Proteins / metabolism* Membrane Potential, Mitochondrial / drug effects Mitochondria / drug effects* Mitochondrial Proteins / metabolism* Phosphorylation RNA Interference RNA, Small Interfering Ribonucleotides / pharmacology bcl-X Protein / metabolism*
IF 5.5
Times Cited 19
WOS Category PHYSIOLOGY CELL BIOLOGY
Resource
Human and Animal Cells HuH-7(RCB1366)