AI Article Synopsis
- Wnt signaling is linked to various human cancers and plays a role in cancer development by promoting the expression of phosphofructokinase 1 platelet isoform (PFKP), which is crucial for glycolysis and the Warburg effect.
- The study found that Wnt3A, not relying on β-catenin, increased PFKP expression and enzyme activity, leading to enhanced cancer cell proliferation and migration.
- Additionally, Wnt3A activated the epidermal growth factor receptor, triggering a pathway that phosphorylated PFKP and further elevated its expression, highlighting its significance in tumor growth driven by Wnt signaling.
Article Abstract
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 β‑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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| http://dx.doi.org/10.3892/or.2021.8185 | DOI Listing |
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