title: EGFR inhibition prevents in vitro tumor growth of salivary adenoid cystic carcinoma.
abstract: BACKGROUND
  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.
  
  
  RESULTS
  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.
  
  
  CONCLUSIONS
  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.
authors.affiliation: Department of Head and Neck Oncology, West China College of Stomatology, Sichuan University, and Department of Thoracic Cancer, West China Hospital, No,14, Section 3, Ren Min Nan Road, Chengdu, 610041, China. maohuangyi@hotmail.com
authors.forename: Yi
authors.initials: Y
authors.lastname: Huang
authors.forename: Tao
authors.initials: T
authors.lastname: Yu
authors.forename: Xiaoyue
authors.initials: X
authors.lastname: Fu
authors.forename: Jiao
authors.initials: J
authors.lastname: Chen
authors.forename: Ying
authors.initials: Y
authors.lastname: Liu
authors.forename: Chunjie
authors.initials: C
authors.lastname: Li
authors.forename: Yichao
authors.initials: Y
authors.lastname: Xia
authors.forename: Zhuoyuan
authors.initials: Z
authors.lastname: Zhang
authors.forename: Longjiang
authors.initials: L
authors.lastname: Li
mesh_terms: D061067:Antibodies, Monoclonal, Humanized / Q000494:pharmacology; D000970:Antineoplastic Agents / Q000494:pharmacology; D003528:Carcinoma, Adenoid Cystic / Q000378:metabolism / Q000473:pathology; D045744:Cell Line, Tumor; D002465:Cell Movement / Q000187:drug effects; D049109:Cell Proliferation / Q000187:drug effects; D004815:Epidermal Growth Factor / Q000494:pharmacology; D066246:ErbB Receptors / Q000037:antagonists & inhibitors / Q000378:metabolism*; D059585:G1 Phase Cell Cycle Checkpoints / Q000187:drug effects; D006801:Humans; D019394:Ki-67 Antigen / Q000378:metabolism; D020780:Matrix Metalloproteinase 9 / Q000378:metabolism; D020929:Mitogen-Activated Protein Kinase Kinases / Q000378:metabolism; D010766:Phosphorylation; D000071250:Snail Family Transcription Factors; D014157:Transcription Factors / Q000378:metabolism; D015854:Up-Regulation / Q000187:drug effects
chemical_list: D061067:Antibodies, Monoclonal, Humanized; D000970:Antineoplastic Agents; D019394:Ki-67 Antigen; D000071250:Snail Family Transcription Factors; D014157:Transcription Factors; D004815:Epidermal Growth Factor; C501466:nimotuzumab; D066246:ErbB Receptors; D020929:Mitogen-Activated Protein Kinase Kinases; D020780:Matrix Metalloproteinase 9