Journal
ONCOLOGY REPORTS
Volume 46, Issue 5, Pages -Publisher
SPANDIDOS PUBL LTD
DOI: 10.3892/or.2021.8185
Keywords
Wnt; epidermal growth factor receptor; transactivation; AKT; phosphofructokinase 1 platelet isoform; phosphorylation
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Funding
- Dong-A University research fund
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The study found that Wnt signaling can induce the expression of PFKP independently of beta-catenin, increase PFK enzyme activity, and promote the Warburg effect, cell proliferation, colony formation, and cancer cell migration through PFKP S386 phosphorylation.
The activation of Wnt signaling has been detected in various types of human cancer and has been shown to be associated with cancer development. In the present study, it was revealed that Wnt signaling induced the expression of phosphofructokinase 1 platelet isoform (PFKP), which has been reported to catalyze a rate-limiting reaction in glycolysis and is important for the Warburg effect, proliferation, colony formation and cancer cell migration. Moreover, it was demonstrated that Wnt3A induced PFKP expression in a beta-catenin-independent manner, resulting in increased PFK enzyme activity. Wnt3A-induced epidermal growth factor receptor transactivation activated PI3K/AKT, which stabilized PFKP through PFKP S386 phosphorylation and subsequent PFKP upregulation. Wnt3A-induced PFKP S386 phosphorylation increased PFKP expression and promoted the Warburg effect, cell proliferation, colony formation and the migratory ability of cancer cells. On the whole, the findings of the present study underscore the potential role of PFKP in Wnt signaling-induced tumor development.
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