Tropical Journal of Pharmaceutical Research

Original Research Article | OPEN ACCESS

FOXP2 regulates the proliferation, migration, and apoptosis of thyroid carcinoma cells via Wnt/β-catenin signaling pathway

Hui Zou¹, Caiyi Tang², Hao Chen³

¹Department of Hepatobiliary Pancreatic Mammary Thyroid, People's Hospital of Kai Zhou District, Chongqing 400000; ²Division of Public Health Management, The People's Hospital of Kai Zhou District, Chongqing 400000; ³Department of Ultrasound Medicine, Lishui People's Hospital, The Sixth Affiliated Hospital of Wenzhou Medical University, Lishui, Zhejiang Province 323000, China.

For correspondence:- Hao Chen Email: chenhao_0322@163.com Tel:+865782780098

Accepted: 27 July 2021 Published: 31 August 2021

Citation: Zou H, Tang C, Chen H. FOXP2 regulates the proliferation, migration, and apoptosis of thyroid carcinoma cells via Wnt/β-catenin signaling pathway. Trop J Pharm Res 2021; 20(8):1609-1614 doi: 10.4314/tjpr.v20i8.9

© 2021 The authors.
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Abstract

Purpose: To determine the effect of Forkhead box P2 (FOXP2) on thyroid carcinoma cell growth and metastasis.

Methods: expression of FOXP2 in thyroid carcinoma cells was determined using quantitative reverse transcription-polymerase chain reaction (qRT-PCR) and western blot. The 3-[4,5-dimethylthiazol-2-yl]-2,5 diphenyl tetrazolium bromide (MTT) was applied to evaluate cell viability, while cell migration and invasion were assessed by wound healing and Transwell assays, respectively. Flow cytometry and western blot were conducted to investigate cell apoptosis. The underlying mechanisms were investigated using western blot assay.

Results: expression of FOXP2 was lower in primary thyroid carcinoma tissues than in normal tissues based on data from the TCGA database. Similarly, FOXP2 was lower in thyroid carcinoma cells at the mRNA and protein levels. Ectopic FOXP2 expression decreased cell viability, and retarded the migration and invasion of thyroid carcinoma cells. FOXP2 overexpression in thyroid carcinoma cells led to down-regulated expression of matrix metallopeptidase (MMP) 2, MMP 9, and proliferating cell nuclear antigen (PCNA), as well as induction of cell apoptosis. Moreover, FOXP2 overexpression resulted in enhanced Bax expression while Bcl-2 was reduced. Ectopic expression of FOXP2 decreased β-catenin, c-myc, and cyclin D1 in thyroid carcinoma cells.

Conclusion: FOXP2 suppresses the proliferation and metastasis of thyroid carcinoma cells, but promotes apoptosis through suppression of the Wnt/β-catenin signaling pathway. These results provide an insight that may lead to the development of a novel potential therapeutic strategy for treating thyroid carcinoma.

Keywords: FOXP2, Cell proliferation, Metastasis, Apoptosis, Thyroid carcinoma, Wnt/?-catenin