Journal
NATURE COMMUNICATIONS
Volume 8, Issue -, Pages -Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/ncomms14374
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Funding
- National Research Foundation of Korea - Korea government (MSIP) [NRF-2012M3A9B2052523, NRF-2014R1A2A1A05004670, NRF-2016R1E1A1A01942724]
- National Research Foundation of Korea - Korea government (MOE) [NRF-2014R1A6A3A04055110]
- National R&D Program for Cancer Control, Ministry for Health, Welfare and Family Affairs, Republic of Korea [1420310]
- National Research Council of Science Technology [CAP-2012-2-KBSI]
- Korea Basic Science Institute [C36705]
- National Cancer Center of Korea [NCC1410670]
- Korea Health Promotion Institute [1420310] Funding Source: Korea Institute of Science & Technology Information (KISTI), National Science & Technology Information Service (NTIS)
- National Research Council of Science & Technology (NST), Republic of Korea [CAP-12-02-KBSI, C37700] Funding Source: Korea Institute of Science & Technology Information (KISTI), National Science & Technology Information Service (NTIS)
- National Research Foundation of Korea [21A20132212238, 2014R1A2A1A05004670, 2012M3A9B2052523, 2014R1A6A3A04055110] Funding Source: Korea Institute of Science & Technology Information (KISTI), National Science & Technology Information Service (NTIS)
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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.
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