Tropical Journal of Pharmaceutical Research

Original Research Article | OPEN ACCESS

MFAP2 contributes to the proliferation and motility of lung cancer cells via Wnt/β-catenin pathway

Xiuyun He¹, Yunfeng Qiao²

¹Department of Oncology, Hospital of Chengdu University of Traditional Chinese Medicine, Chengdu, Sichuan Province 610072, China; ²Department of Oncology, Renmin Hospital of Wuhan University, Wuhan, Hubei Province 430060, China.

For correspondence:- Yunfeng Qiao Email: qiaoyunfeng11207@163.com Tel:+8618171422505

Accepted: 15 April 2022 Published: 31 May 2022

Citation: He X, Qiao Y. MFAP2 contributes to the proliferation and motility of lung cancer cells via Wnt/β-catenin pathway. Trop J Pharm Res 2022; 21(5):915-920 doi: 10.4314/tjpr.v21i5.1

© 2022 The authors.
This is an Open Access article that uses a funding model which does not charge readers or their institutions for access and distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0) and the Budapest Open Access Initiative (http://www.budapestopenaccessinitiative.org/read), which permit unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited..

Abstract

Purpose: To measure microfibrillar-associated protein 2 (MFAP2) expression levels in lung cancer and identify its role in lung cancer.

Methods: Immunoblots and PCR were used to determine the expression of MFAP2 in lung cancer cell lines. The effects of MFAP2 on the viability and apoptosis of lung cancer cells were evaluated by CCK-8, colony formation, and flow cytometry (FCM) assays, while wound healing and Transwell assays were used to assess the effects of MFAP2 on the motility and epithelial-mesenchymal transition (EMT) of lung cancer cells. Immunoblot assays were also performed to determine the effect of MFAP2 on the Wnt/β-catenin axis in lung cancer cells.

Results: MFAP2 was highly expressed in lung cancer cells. Depletion of MFAP2 suppressed the viability and stimulated apoptosis in these cells (p < 0.01). In addition, knockdown of MFAP2 suppressed the motility and EMT of lung cancer cells (p < 0.01). MFAP2 mediated the Wnt/β-catenin axis and affected the viability and motility of lung cancer cells.

Conclusion: MFAP2 is a promising target for lung cancer treatment.

Keywords: Microfibrillar-associated protein 2 (MFAP2), Lung cancer, Viability, Motility, Wnt/?-catenin pathway