LKB1-AMPK axis revisited.
The LKB1 tumor suppressor encodes a serine-threonine kinase whose substrates control cell metabolism, polarity, and motility. LKB1 is a major mediator of the cellular response to energy stress via activation of the master regulator of energy homeostasis, AMPK. While mutational inactivation of LKB1 promotes the development of many types of epithelial cancer, a recent report in Nature by Jeon et al. demonstrates that the LKB1-AMPK pathway can also have an unexpected positive role in tumorigenesis, acting to maintain metabolic homeostasis and attenuate oxidative stress thereby supporting the survival of cancer cells.
Massachusetts General Hospital Cancer Center, Harvard Medical School, Boston, MA 02114, USA.
Filippos
F
Kottakis
Nabeel
N
Bardeesy
D000091162:AMP-Activated Protein Kinase Kinases; D055372:AMP-Activated Protein Kinases / Q000378:metabolism*; D000103:Acetyl-CoA Carboxylase / Q000378:metabolism; D000123:Acetyltransferases / Q000378:metabolism; D045744:Cell Line, Tumor; D004734:Energy Metabolism; D006801:Humans; D009154:Mutation; D009249:NADP / Q000378:metabolism; D018384:Oxidative Stress; D017346:Protein Serine-Threonine Kinases / Q000235:genetics / Q000378:metabolism*; D015398:Signal Transduction; D058570:TOR Serine-Threonine Kinases / Q000378:metabolism
D009249:NADP; D000123:Acetyltransferases; C055210:aminoglycoside N1-acetyltransferase; D017346:Protein Serine-Threonine Kinases; C109790:STK11 protein, human; D058570:TOR Serine-Threonine Kinases; D000091162:AMP-Activated Protein Kinase Kinases; D055372:AMP-Activated Protein Kinases; C520105:ACACB protein, human; D000103:Acetyl-CoA Carboxylase