Unknown

Dataset Information

0

Requirement for ribosomal protein S6 kinase 1 to mediate glycolysis and apoptosis resistance induced by Pten deficiency.


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-1?, and HIF-1? 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.

SUBMITTER: Tandon P 

PROVIDER: S-EPMC3038712 | biostudies-literature | 2011 Feb

REPOSITORIES: biostudies-literature

altmetric image

Publications

Requirement for ribosomal protein S6 kinase 1 to mediate glycolysis and apoptosis resistance induced by Pten deficiency.

Tandon Preeti P   Gallo Catherine A CA   Khatri Shikha S   Barger Jennifer F JF   Yepiskoposyan Hasmik H   Plas David R DR  

Proceedings of the National Academy of Sciences of the United States of America 20110124 6


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  ...[more]

Similar Datasets

| S-EPMC10758423 | biostudies-literature
| S-EPMC7610917 | biostudies-literature
| S-EPMC8175238 | biostudies-literature
| S-EPMC2685676 | biostudies-literature
| S-EPMC4954603 | biostudies-literature
| S-EPMC3913359 | biostudies-literature
| S-EPMC1223513 | biostudies-other
2024-07-09 | GSE218683 | GEO
2024-07-09 | GSE218684 | GEO
2024-07-09 | GSE218682 | GEO