Abstract
Does the LKB1-AMPK (AMP-activated protein kinase) pathway act to suppress tumorigenesis or to rescue cancer cells from metabolic collapse? New work from the Alessi laboratory in this issue of the Biochemical Journal shows conclusively that AMPK activators delay the growth of tumours that occur spontaneously in PTEN (phosphatase and tensin homologue deleted on chromosome 10) heterozygous mice.
MeSH terms
-
AMP-Activated Protein Kinases
-
Adenylate Kinase / genetics
-
Adenylate Kinase / metabolism*
-
Animals
-
Enzyme Activation
-
Humans
-
Mechanistic Target of Rapamycin Complex 1
-
Mice
-
Multiprotein Complexes
-
Neoplasms* / enzymology
-
Neoplasms* / therapy
-
PTEN Phosphohydrolase / genetics
-
PTEN Phosphohydrolase / metabolism
-
Phosphatidylinositol 3-Kinases / metabolism
-
Protein Kinases / genetics
-
Protein Kinases / metabolism
-
Protein Serine-Threonine Kinases / genetics
-
Protein Serine-Threonine Kinases / metabolism
-
Proteins
-
Proto-Oncogene Proteins c-akt / metabolism
-
Signal Transduction / physiology
-
TOR Serine-Threonine Kinases
-
Transcription Factors / genetics
-
Transcription Factors / metabolism
Substances
-
Multiprotein Complexes
-
Proteins
-
Transcription Factors
-
Protein Kinases
-
MTOR protein, human
-
mTOR protein, mouse
-
Mechanistic Target of Rapamycin Complex 1
-
Protein Serine-Threonine Kinases
-
Proto-Oncogene Proteins c-akt
-
Stk11 protein, mouse
-
TOR Serine-Threonine Kinases
-
AMP-Activated Protein Kinases
-
Adenylate Kinase
-
PTEN Phosphohydrolase