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.

中文翻译：

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Wnt 信号部分通过磷酸果糖激酶 1 血小板同种型上调促进肿瘤发展。

已在各种类型的人类癌症中检测到 Wnt 信号的激活，并已证明与癌症的发展有关。在本研究中，发现 Wnt 信号诱导磷酸果糖激酶 1 血小板同种型 (PFKP) 的表达，据报道，PFKP 催化糖酵解中的限速反应，对 Warburg 效应、增殖、集落形成和癌症很重要细胞迁移。此外，已经证明 Wnt3A 以不依赖 β-catenin 的方式诱导 PFKP 表达，导致 PFK 酶活性增加。Wnt3A 诱导的表皮生长因子受体反式激活激活 PI3K/AKT，通过 PFKP S386 磷酸化和随后的 PFKP 上调稳定 PFKP。Wnt3A 诱导的 PFKP S386 磷酸化增加了 PFKP 表达并促进了 Warburg 效应、细胞增殖、集落形成和癌细胞的迁移能力。总的来说，本研究的结果强调了 PFKP 在 Wnt 信号诱导的肿瘤发展中的潜在作用。