Profilin 2 Promotes Proliferation and Metastasis of Head and Neck Cancer Cells by Regulating PI3K/AKT/β-Catenin Signaling Pathway
| Autor: | Jiayu Wu, Songhe Jiang, Peng Zhou, Jie Chen, Shengcun Li, Guanhu Yang, Qiaoyun Wu, Yu Song, Yangxinzi Xu, Jingjing Yue, Wenzhan Tu, Kecheng Zhou |
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| Rok vydání: | 2019 |
| Předmět: |
0301 basic medicine
Cancer Research Proliferation Apoptosis Profilin 2 (PFN2) Biology Article Metastasis Mice Phosphatidylinositol 3-Kinases Profilins 03 medical and health sciences 0302 clinical medicine Nude mouse Invasion Downregulation and upregulation Cell Movement Cell Line Tumor medicine Animals Humans Neoplasm Metastasis Protein kinase B beta Catenin Migration PI3K/Akt/β-catenin pathway PI3K/AKT/mTOR pathway Cell Proliferation Gene knockdown Head and neck cancer (HNSC) General Medicine biology.organism_classification medicine.disease Up-Regulation 030104 developmental biology Oncology Head and Neck Neoplasms 030220 oncology & carcinogenesis Cancer research Heterografts Phosphorylation Signal transduction Proto-Oncogene Proteins c-akt Signal Transduction |
| Zdroj: | Oncology Research |
| ISSN: | 0965-0407 |
| Popis: | Profilin 2 (PFN2) was found to be mainly expressed in neurons and involved in the development of the brain. In recent years, emerging evidence indicated that PFN2 is also significantly upregulated in various cancers including head and neck cancer (HNSC) and influences cancer cell proliferation, migration, and invasion. However, the role of PFN2 in HNSC development and progression remains unclear. The aim of our study was to investigate the role of PFN2 in the development of HNSC and its possible molecular mechanisms. Bioinformatics showed that increased expression of PFN2 in tumors correlated highly with poor prognosis of HNSC patients. Our results indicated that PFN2 was highly expressed in HNSC tissues and in HNSC cell lines. Knockdown of PFN2 inhibited proliferation, invasion, and migration of HNSC cells, while PFN2 overexpression produced the opposite effects. Using a nude mouse xenograft model, we substantiated the tumor-promoting effect of PFN2 on HNSC in vivo. Furthermore, we found that PFN2 downregulation reduced the phosphorylation of Akt and GSK-3β and reduced the expression of β-catenin in HNSC cells. The opposite was observed when PFN2 was overexpressed. Collectively, these results suggest that PFN2 promotes the proliferation and metastasis of HNSC by activating the PI3K/Akt/β-catenin signaling pathway. Although further validation is needed, we speculate that PFN2 plays a crucial role in HNSC and may be a promising therapeutic target and prognostic biomarker. |
| Databáze: | OpenAIRE |
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