Open Access Open Badges Research article

EGFR inhibition prevents in vitro tumor growth of salivary adenoid cystic carcinoma

Yi Huang12, Tao Yu14, Xiaoyue Fu3, Jiao Chen2, Ying Liu12, Chunjie Li12, Yichao Xia12, Zhuoyuan Zhang12 and Longjiang Li1*

Author Affiliations

1 Department of Head and Neck Oncology, West China College of Stomatology, Sichuan University, No.14, Section 3, Ren Min Nan Road, Chengdu, 610041, China

2 State Key Laboratory of Oral Diseases, West China Collegel of Stomatology, Sichuan University, Chengdu, China

3 Department of Thoracic Cancer, West China Hospital of Sichuan University, Chengdu, China

4 Department of Head and Neck Oncology, Sichuan Cancer Hospital, No. 55, Sec. 4, Renminnan Road, Chengdu, Sichuan, 610041, People’s Republic of China

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BMC Cell Biology 2013, 14:13  doi:10.1186/1471-2121-14-13

Published: 9 March 2013



Epidermal growth factor receptor (EGFR) is involved in the development of many human malignant tumors and plays an important role in tumor growth and metastasis. Antagonists of EGFR can suppress the growth of several malignancies; however, their therapeutic effect in adenoid cystic carcinoma (ACC) is controversial.


The increased proliferation of two ACC cell lines induced by EGF-treatment was reversed by nimotuzumab. Regardless of EGF stimulation, nimotuzumab-treated ACC cells were arrested in G1 phase and showed decreased expression of Ki67. In addition, EGF activated the MAPK-dependent pathway and up-regulated the expression of matrix metalloproteinase-9 and Snail, enhancing the invasive potential of an ACC cell line (ACC-M). The effects of EGF were down-regulated by nimotuzumab treatment.


These results suggest that nimotuzumab can inhibit the growth and invasion of ACC cells induced by EGF, probably through inactivation of ERK phosphorylation. Thus, nimotuzumab should be considered as a promising novel agent for the treatment of ACC.

Epidermal growth factor receptor (EGFR); Adenoid cystic carcinoma (ACC); Nimotuzumab; Monoclonal antibody; Matrix metalloproteinase (MMP); Epithelial- mesenchymal transition (EMT); Invasion; Cancer therapy