title: MCP1-Induced Epithelial-Mesenchymal Transition in Head and Neck Cancer by AKT Activation.
abstract: OBJECTIVE
  To explore whether monocyte chemotactic protein-1 (MCP1) is associated with the epithelial-mesenchymal transition (EMT) and neck metastases in head and neck cancer (HNC).
  
  
  METHODS
  MCP1 and its related protein were evaluated using western blotting, and a migration assay for HNC cell lines. Thirty-five patients with HNC were recruited for the evaluation of MCP1 expression and pathologically-proven neck metastases from their tissue specimens.
  
  
  RESULTS
  MCP1 changed the phenotype of OML-1 cells to a spindle shape, with increased mobility. In OML3 cells, MCP1 knockdown with siRNA blocked EMT. Activation of protein kinase B (AKT) was positively associated with the EMT phenotype, and this transition was abrogated with a phosphoinositide 3 kinase (PI3K) inhibitor. By comparing clinical outcomes, the histological MCP1 score was associated with pathological neck metastases (p=0.027).
  
  
  CONCLUSIONS
  The overexpression of MCP1 in HNC cells may partially induce EMT through the AKT pathway. A high cellular expression of MCP1 was associated with pathological neck metastases.
authors.affiliation: Department of Otolaryngology, Dalin Tzu Chi Hospital, Buddhist Tzu Chi Medical Foundation, Chiayi, Taiwan, R.O.C. School of Medicine, Tzu Chi University, Hualian, Taiwan, R.O.C.
authors.forename: Ching-Chih
authors.initials: CC
authors.lastname: Lee
authors.affiliation: Department of Otolaryngology, Dalin Tzu Chi Hospital, Buddhist Tzu Chi Medical Foundation, Chiayi, Taiwan, R.O.C. School of Medicine, Tzu Chi University, Hualian, Taiwan, R.O.C.
authors.forename: Hsu-Chueh
authors.initials: HC
authors.lastname: Ho
authors.affiliation: School of Medicine, Tzu Chi University, Hualian, Taiwan, R.O.C. Division of Hematology-Oncology, Department of Internal Medicine, Dalin Tzu Chi Hospital, Buddhist Tzu Chi Medical Foundation, Chiayi, Taiwan, R.O.C.
authors.forename: Yu-Chieh
authors.initials: YC
authors.lastname: Su
authors.affiliation: School of Medicine, Tzu Chi University, Hualian, Taiwan, R.O.C. Department of Radiation Oncology, Dalin Tzu Chi Hospital, Buddhist Tzu Chi Medical Foundation, Chiayi, Taiwan, R.O.C.
authors.forename: Moon-Sing
authors.initials: MS
authors.lastname: Lee
authors.affiliation: School of Medicine, Tzu Chi University, Hualian, Taiwan, R.O.C. Department of Radiation Oncology, Dalin Tzu Chi Hospital, Buddhist Tzu Chi Medical Foundation, Chiayi, Taiwan, R.O.C.
authors.forename: Shih-Kai
authors.initials: SK
authors.lastname: Hung
authors.affiliation: Department of Medical Research, Dalin Tzu Chi Hospital, Buddhist Tzu Chi Medical Foundation, Chiayi, Taiwan, R.O.C. kumar1119@yahoo.com.tw.
authors.forename: Chun-Hsuan
authors.initials: CH
authors.lastname: Lin
mesh_terms: D000328:Adult; D045744:Cell Line, Tumor; D018932:Chemokine CCL2 / Q000235:genetics*; D058750:Epithelial-Mesenchymal Transition / Q000235:genetics*; D005260:Female; D015972:Gene Expression Regulation, Neoplastic / Q000187:drug effects; D006258:Head and Neck Neoplasms / Q000235:genetics* / Q000473:pathology / Q000556:secondary; D006801:Humans; D008297:Male; D008875:Middle Aged; D051058:Oncogene Protein v-akt / Q000096:biosynthesis* / Q000235:genetics; D019869:Phosphatidylinositol 3-Kinases / Q000096:biosynthesis / Q000235:genetics; D047428:Protein Kinase Inhibitors / Q000008:administration & dosage; D034741:RNA, Small Interfering; D015398:Signal Transduction / Q000235:genetics; D015533:Transcriptional Activation / Q000235:genetics
chemical_list: C111835:CCL2 protein, human; D018932:Chemokine CCL2; D047428:Protein Kinase Inhibitors; D034741:RNA, Small Interfering; D019869:Phosphatidylinositol 3-Kinases; D051058:Oncogene Protein v-akt
keywords: AKT; MCP1; epithelial–mesenchymal transition; head and neck cancer