Open Access

ARTICLE

Profilin 2 Promotes Proliferation and Metastasis of Head and Neck Cancer Cells by Regulating PI3K/AKT/b-Catenin Signaling Pathway

Kecheng Zhou^*†1, Jie Chen^*†1, Jiayu Wu^*†1, Yangxinzi Xu^‡, Qiaoyun Wu^*†, Jingjing Yue^*†, Yu Song^§, Shengcun Li^*†, Peng Zhou^¶, Wenzhan Tu^*†, Guanhu Yang^*†, Songhe Jiang^*†

* Department of Physical Medicine and Rehabilitation, The Second Affiliated Hospital and Yuying Children’s Hospital of Wenzhou Medical University, Wenzhou, Zhejiang, P.R. China
† Integrative and Optimized Medicine Research Center, China–USA Institute for Acupuncture and Rehabilitation, Wenzhou Medical University, Wenzhou, Zhejiang, P.R. China
‡ Department of Physiology and Pathophysiology, University of Manitoba, Winnipeg, Manitoba, Canada
§ Institute of Clinical Pharmacology, Anhui Medical University, Key Laboratory of Anti-inflammatory and Immune Medicine, Ministry of Education, Anhui Collaborative Innovation Center of Anti-inflammatory and Immune Medicine, Hefei, Anhui, P.R. China
¶ Department of Anatomy, Wenzhou Medical University, Wenzhou, Zhejiang, P.R. China

Oncology Research 2019, 27(9), 1079-1088. https://doi.org/10.3727/096504019X15579146061957

Abstract

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-3 and reduced the expression of -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/ -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.

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