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Snail reprograms glucose metabolism by repressing phosphofructokinase PFKP allowing cancer cell survival under metabolic stress

Title
Snail reprograms glucose metabolism by repressing phosphofructokinase PFKP allowing cancer cell survival under metabolic stress
Authors
Kim N.H.Cha Y.H.Lee J.Lee S.-H.Yang J.H.Yun J.S.Cho E.S.Zhang X.Nam M.Kim N.Yuk Y.-S.Cha S.Y.Lee Y.Ryu J.K.Park S.Cheong J.-H.Kang S.W.Kim S.-Y.Hwang G.-S.Yook J.I.Kim H.S.
Ewha Authors
강상원황금숙
SCOPUS Author ID
강상원scopus; 황금숙scopusscopus
Issue Date
2017
Journal Title
Nature Communications
ISSN
2041-1723JCR Link
Citation
vol. 8
Publisher
Nature Publishing Group
Indexed
SCI; SCIE; SCOPUS WOS scopus
Abstract
Dynamic regulation of glucose flux between aerobic glycolysis and the pentose phosphate pathway (PPP) during epithelial-mesenchymal transition (EMT) is not well-understood. Here we show that Snail (SNAI1), a key transcriptional repressor of EMT, regulates glucose flux toward PPP, allowing cancer cell survival under metabolic stress. Mechanistically, Snail regulates glycolytic activity via repression of phosphofructokinase, platelet (PFKP), a major isoform of cancer-specific phosphofructokinase-1 (PFK-1), an enzyme involving the first rate-limiting step of glycolysis. The suppression of PFKP switches the glucose flux towards PPP, generating NADPH with increased metabolites of oxidative PPP. Functionally, dynamic regulation of PFKP significantly potentiates cancer cell survival under metabolic stress and increases metastatic capacities in vivo. Further, knockdown of PFKP rescues metabolic reprogramming and cell death induced by loss of Snail. Thus, the Snail-PFKP axis plays an important role in cancer cell survival via regulation of glucose flux between glycolysis and PPP. © The Author(s) 2017.
DOI
10.1038/ncomms14374
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자연과학대학 > 생명과학전공 > Journal papers
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