Requirement for ribosomal protein S6 kinase 1 to mediate glycolysis and apoptosis resistance induced by Pten deficiency.
basic_science · Level V
Where this comes from
- Record sourced from PubMed, PMID 21262837.
- Also identified by DOI 10.1073/pnas.1013629108 and PMC identifier 3038712.
- No licence information is recorded for this record.
- Because redistribution is not established, this page shows the abstract only. Follow the links below for the full text.
Abstract
Pten inactivation promotes cell survival in leukemia cells by activating glycolytic metabolism. We found that targeting ribosomal protein S6 kinase 1 (S6K1) in Pten-deficient cells suppressed glycolysis and induced apoptosis. S6K1 knockdown decreased expression of HIF-1α, and HIF-1α was sufficient to restore glycolysis and survival of cells lacking S6K1. In the Pten(fl/fl) Mx1-Cre(+) mouse model of leukemia, S6K1 deletion delayed the development of leukemia. Thus, S6K1 is a critical mediator of glycolytic metabolism, cell survival, and leukemogenesis in Pten-deficient cells.
Medical subject headings
- Apoptosis
- Glycolysis
- Leukemia
- Neoplasm Proteins
- PTEN Phosphohydrolase
- Ribosomal Protein S6 Kinases, 90-kDa