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Stabilized Epithelial Phenotype of Cancer Cells in Primary Tumors Leads to Increased Colonization of Liver Metastasis in Pancreatic Cancer

ABSTRACT: Single-cell RNA-sequencing analyses were performed on unfractionated live cell mixtures or YFP sorted cancer cells from pancreatic tumors or liver mets of KPC;YFP control mice and KPC;SnailKO;TwistKO;YFP mice, so as to investigate the Epithelial-to-Mesenchymal Transition (EMT) of cancer cells in primary tumors and metastases. The effect of cancer-specific knockout of EMT transcription factor Snail and Twist on cancer cell EMT was studied by comparing KPC;YFP control mice and KPC;SnailKO;TwistKO;YFP mice. Each sample was in an individual folder containing the related fastq raw data files.

ORGANISM(S): Mus musculus

PROVIDER: GSE165534 | GEO | 2021/02/11

REPOSITORIES: GEO

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Project description: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 PFKP (phosphofructokinase, platelet), 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.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 PFKP (phosphofructokinase, platelet), 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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Stabilized Epithelial Phenotype of Cancer Cells in Primary Tumors Leads to Increased Colonization of Liver Metastasis in Pancreatic Cancer

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