BACKGROUND: The protein eukaryotic initiation factor 4E (elF4E) binds to messenger ribonucleic acid (mRNA) as the initial step in protein synthesis. Overexpression of elF4E results in upregulation of specific proteins essential to cell growth and division. Overexpression of elF4E has been found in head and neck squamous cell carcinoma (HNSCC) and breast carcinoma. This study's purpose is to determine whether elF4E overexpression is present and associated with elF4E gene amplification in HNSCC. METHODS: Competitive polymerase chain reaction (PCR) was performed on eight HNSCC and seven intraoral benign lesions to determine the copy number of elF4E relative to a reference gene, gastrin. Western blots were performed to quantify elF4E protein expression. RESULTS: All eight HNSCC specimens demonstrated significant (p < .005) overexpression of elF4E protein (14.1+/-10.4) and elF4E gene amplification (4.5+/-1.2). Benign tissue did not exhibit elF4E protein overexpression or gene amplification. CONCLUSIONS: Overexpression and associated gene amplification of elF4E were present in HNSCC but not in benign tissue. Gene amplification of elF4E may be an important mechanism for elF4E overexpression.
BACKGROUND: The protein eukaryotic initiation factor 4E (elF4E) binds to messenger ribonucleic acid (mRNA) as the initial step in protein synthesis. Overexpression of elF4E results in upregulation of specific proteins essential to cell growth and division. Overexpression of elF4E has been found in head and neck squamous cell carcinoma (HNSCC) and breast carcinoma. This study's purpose is to determine whether elF4E overexpression is present and associated with elF4E gene amplification in HNSCC. METHODS: Competitive polymerase chain reaction (PCR) was performed on eight HNSCC and seven intraoral benign lesions to determine the copy number of elF4E relative to a reference gene, gastrin. Western blots were performed to quantify elF4E protein expression. RESULTS: All eight HNSCC specimens demonstrated significant (p < .005) overexpression of elF4E protein (14.1+/-10.4) and elF4E gene amplification (4.5+/-1.2). Benign tissue did not exhibit elF4E protein overexpression or gene amplification. CONCLUSIONS: Overexpression and associated gene amplification of elF4E were present in HNSCC but not in benign tissue. Gene amplification of elF4E may be an important mechanism for elF4E overexpression.
Authors: Alex Kentsis; Ivan Topisirovic; Biljana Culjkovic; Ling Shao; Katherine L B Borden Journal: Proc Natl Acad Sci U S A Date: 2004-12-15 Impact factor: 11.205