Imperial College London
Portrait Picture

ProfessorHectorKeun

Faculty of Medicine, Department of Surgery & Cancer

Professor of Biochemistry
 
 
 
//

Contact

 

+44 (0)20 7594 3161h.keun

 
 
//

Location

 

officesInstitute of Reproductive and Developmental BiologyHammersmith Campus

//

Summary

 

Publications

Citation

BibTex format

@article{Koufaris:2016:10.1021/acs.jproteome.6b00188,
author = {Koufaris, C and Gallage, S and Yang, T and Lau, CH and Valbuena, GN and Keun, HC},
doi = {10.1021/acs.jproteome.6b00188},
journal = {Journal of Proteome Research},
pages = {2618--2625},
title = {Suppression of MTHFD2 in MCF-7 Breast Cancer Cells Increases Glycolysis, Dependency on Exogenous Glycine, and Sensitivity to Folate Depletion},
url = {http://dx.doi.org/10.1021/acs.jproteome.6b00188},
volume = {15},
year = {2016}
}
Download

RIS format (EndNote, RefMan)

TY  - JOUR
AB  - Methylenetetrahydrofolate dehydrogenase (NAD(P)+ dependent) 2, methenyltetrahydrofolate cyclohydrolase (MTHFD2) is a mitochondrial enzyme involved in folate metabolism. A number of recent studies have highlighted this enzyme as being highly expressed in many solid tumors, including breast cancer, and to be correlated with poor survival. However, the metabolic functions of MTHFD2 in cancer cells have not been well-defined. To investigate the function of MTHFD2 in breast cancer cells, we generated and characterized MCF-7 cells with stable suppression of MTHFD2 expression using a combination of cellular assays and metabolic profiling. Loss of MTHFD2 caused MCF7 cells to become glycine auxotrophs, that is, reliant on exogenous glycine, and more sensitive to exogenous folate depletion. Another prominent metabolic alteration observed as a consequence of MTHFD2 suppression was a more glycolytic phenotype, consistent with widespread modifications of cellular metabolism. Collectively, these data suggest that targeting MTHFD2 activity is likely to influence multiple metabolic pathways in breast cancer and could be combined with a range of antimetabolite therapies.
AU  - Koufaris,C
AU  - Gallage,S
AU  - Yang,T
AU  - Lau,CH
AU  - Valbuena,GN
AU  - Keun,HC
DO  - 10.1021/acs.jproteome.6b00188
EP  - 2625
PY  - 2016///
SN  - 1535-3907
SP  - 2618
TI  - Suppression of MTHFD2 in MCF-7 Breast Cancer Cells Increases Glycolysis, Dependency on Exogenous Glycine, and Sensitivity to Folate Depletion
T2  - Journal of Proteome Research
UR  - http://dx.doi.org/10.1021/acs.jproteome.6b00188
UR  - http://hdl.handle.net/10044/1/37538
VL  - 15
ER  -
Download