Related Experiment Video
Updated: Jul 2, 2025
05:39
Spontaneous Murine Model of Anaplastic Thyroid Cancer
Published on: February 3, 2023
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PFKFB3 facilitates cell proliferation and migration in anaplastic thyroid carcinoma via the WNT/β-catenin signaling
Jinmei Deng1, Yanglei Cheng2, Hai Li2
1Internal Medicine Department, The First Affiliated Hospital of Sun Yat-sen University, 58 Zhongshan Road II, Guangzhou, 510080, Guangdong, China.
Endocrine
|February 20, 2024
Summary
6-phosphofructo-2-kinase/fructose-2,6-biphosphatase3 (PFKFB3) drives anaplastic thyroid carcinoma (ATC) cell growth and metastasis by activating the WNT/β-catenin pathway and aerobic glycolysis. Inhibiting PFKFB3 suppressed tumor growth in vivo.
Area of Science:
- Oncology
- Molecular Biology
- Biochemistry
Background:
- 6-phosphofructo-2-kinase/fructose-2,6-biphosphatase3 (PFKFB3) is implicated in various cancers.
- Its role in anaplastic thyroid carcinoma (ATC) is not well understood.
Purpose of the Study:
- To investigate the biological functions and molecular mechanisms of PFKFB3 in ATC.
- To evaluate the therapeutic potential of PFKFB3 inhibition in ATC.
Main Methods:
- Analysis of PFKFB3 expression in ATC tissues using public datasets and immunohistochemistry.
- In vitro assays to assess the impact of PFKFB3 modulation on ATC cell proliferation and migration.
- Western blotting, luciferase assays, and in vivo xenograft models to elucidate molecular mechanisms and therapeutic efficacy.
Main Results:
- PFKFB3 expression is significantly elevated in ATC.
- PFKFB3 overexpression promotes ATC cell proliferation, migration, and activates the WNT/β-catenin pathway.
- PFKFB3 inhibition or downregulation suppressed tumor growth and lactate production in vitro and in vivo.
Conclusions:
- PFKFB3 enhances ATC cell proliferation and migration through the WNT/β-catenin signaling pathway.
- PFKFB3 is a key regulator of aerobic glycolysis in ATC.
- PFKFB3 inhibition represents a potential therapeutic strategy for ATC.
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