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Human epithelial growth factor receptor 2 in human salivary carcinoma ex pleomorphic adenoma: a potential therapeutic target

Authors Xia L, Wang Y, Hu Y, Zhang C, Gu T, Wang L, Li J, Yu W, Tian Z

Received 4 August 2018

Accepted for publication 7 October 2018

Published 30 November 2018 Volume 2018:10 Pages 6571—6579

DOI https://doi.org/10.2147/CMAR.S182652

Checked for plagiarism Yes

Review by Single-blind

Peer reviewers approved by Dr Amy Norman

Peer reviewer comments 2

Editor who approved publication: Dr Beicheng Sun


Liang Xia,1,2,* Yang Wang,1,* Yuhua Hu,1,* Chunye Zhang,1 Ting Gu,1 Lizhen Wang,1 Jiang Li,1 Wenwen Yu,2 Zhen Tian1

1Department of Oral Pathology, Ninth People’s Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai Key Laboratory of Stomatology, Shanghai 200011, People’s Republic of China; 2Department of Oral and Cranio-maxillofacial Surgery, Ninth People’s Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai Key Laboratory of Stomatology, Shanghai 200011, People’s Republic of China

*These authors contributed equally to this work

Background: To inhibit human epithelial growth factor receptor 2 (HER2) in salivary carcinoma ex pleomorphic adenoma (CXPA) and investigate the effects on tumor cell proliferation, cell cycle, and apoptosis. To assess the possibility of blocking HER2 to improve the malignant biological behavior of CXPA.
Materials and methods: HER2 expression and amplification were examined using an immunofluorescence assay and fluorescence in situ hybridization in 2 CXPA cell lines (SM-AP1 and SM-AP4 cells). The effects on tumor cell proliferation, cell cycle, apoptosis, and HER2 downstream pathways were verified after the application of a HER2 inhibitor.
Results: HER2 was overexpressed and amplified in SM-AP1 and SM-AP4 cell lines. After blocking HER2, the tumor proliferation and cell cycle were significantly induced, and the apoptosis process was activated. Moreover, the downstream pathways PI3K/AKT and MAPK/ERK were significantly inhibited.
Conclusion: HER2 was overexpressed and amplified in CXPA cell lines and might thus play an important role in tumor development. Inhibiting HER2 may be a novel targeted therapy for poor biological behavior of CXPA.

Keywords: HER2, amplification, carcinoma ex pleomorphic adenoma, proliferation, apoptosis, target therapy

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