Abstract:
:Neoplastic cells metabolize higher amounts of glucose relative to normal cells in order to cover increased energetic and anabolic needs. Inhibition of the glycolytic enzyme 6-phosphofructo-2-kinase/fructose-2,6-bisphosphatase 3 (PFKFB3) diminishes cancer cell proliferation and tumour growth in animals. In this work, we investigate the crosstalk between PFKFB3 and TIGAR (TP53-Induced Glycolysis and Apoptosis Regulator), a protein known to protect cells from oxidative stress. Our results show consistent TIGAR induction in HeLa cells in response to PFKFB3 knockdown. Upon PFKFB3 silencing, cells undergo oxidative stress and trigger Akt phosphorylation. This leads to induction of a TIGAR-mediated prosurvival pathway that reduces both oxidative stress and cell death. As TIGAR is known to have a role in DNA repair, it could serve as a potential target for the development of effective antineoplastic therapies.
journal_name
FEBS Lettjournal_title
FEBS lettersauthors
Simon-Molas H,Calvo-Vidal MN,Castaño E,Rodríguez-García A,Navarro-Sabaté À,Bartrons R,Manzano Adoi
10.1002/1873-3468.12338subject
Has Abstractpub_date
2016-09-01 00:00:00pages
2915-26issue
17eissn
0014-5793issn
1873-3468journal_volume
590pub_type
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