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Medical AI Inquiry: You was designed to assist in medical decision-making based on the provided user questions. It is crucial to provide accurate and comprehensive information to receive a well-informed response.  Labels: OBJECTIVE, METHODS, RESULTS. Meshes: AMP-Activated Protein Kinases, Adenosine, Aminoimidazole Carboxamide, Apoptosis, Cell Line, Tumor, Humans, Intracellular Signaling Peptides and Proteins, Membrane Potential, Mitochondrial, Mitochondria, Mitochondrial Proteins, Phosphorylation, RNA Interference, RNA, Small Interfering, Ribonucleotides, bcl-X Protein.
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Does adenosine activate AMPK to phosphorylate Bcl-XL responsible for mitochondrial damage and DIABLO release in HuH-7 cells? Context: 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. 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. 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).
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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. Final Decision: yes