CXCL12 promotes glycolytic reprogramming in acute myeloid leukemia cells via the CXCR4/mTOR axis

Leukemia. 2016 Aug;30(8):1788-92. doi: 10.1038/leu.2016.58. Epub 2016 Mar 8.

Authors

M Braun¹, M Qorraj¹, M Büttner², F A Klein³, D Saul¹, M Aigner¹, W Huber³, A Mackensen¹, R Jitschin¹, D Mougiakakos¹

Affiliations

¹ Department of Internal Medicine 5, Hematology and Oncology, University of Erlangen-Nuremberg, Erlangen, Germany.
² Institute of Pathology, Department of Nephropathology, University of Erlangen-Nuremberg, Erlangen, Germany.
³ European Molecular Biology Laboratory (EMBL), Heidelberg, Germany.

PMID: 26952837
DOI: 10.1038/leu.2016.58

No abstract available

Publication types

Letter
Research Support, Non-U.S. Gov't

MeSH terms

Cell Line, Tumor
Cellular Reprogramming / physiology*
Chemokine CXCL12 / metabolism*
Glycolysis
Humans
Leukemia, Myeloid, Acute / metabolism*
Leukemia, Myeloid, Acute / pathology
Receptors, CXCR4 / metabolism*
TOR Serine-Threonine Kinases / metabolism*

Substances

CXCL12 protein, human
CXCR4 protein, human
Chemokine CXCL12
Receptors, CXCR4
MTOR protein, human
TOR Serine-Threonine Kinases