Characterization of ten newly-derived human head and neck squamous carcinoma cell lines with special reference to C-erbB proto-oncogene expression

Citation
P. O-charoenrat et al., Characterization of ten newly-derived human head and neck squamous carcinoma cell lines with special reference to C-erbB proto-oncogene expression, ANTICANC R, 21(3B), 2001, pp. 1953-1963
Citations number
31
Categorie Soggetti
Onconogenesis & Cancer Research
Journal title
ANTICANCER RESEARCH
ISSN journal
02507005 → ACNP
Volume
21
Issue
3B
Year of publication
2001
Pages
1953 - 1963
Database
ISI
SICI code
0250-7005(200105/06)21:3B<1953:COTNHH>2.0.ZU;2-7
Abstract
Ten human head and neck squamous carcinoma (HNSCC) cell lines were establis hed in order to study the role of c-erbB signaling pathways in HNSCC progre ssion. Five cell lines were derived from primary tumors at four different s ites, and five were from lymph node metastases in the neck. Two pairs of li nes were derived from the primary tumor and metastatic lymph node in the sa me patient. Basic characteristics including morphology, doubling time, phen otypes, cytogenetic profiles and tumorigenicity in nude mice were described . We examined the expression of c-erbB receptors and ligands in early passa ge new HNSCC lines and compared with five long-term established lines, norm al keratinocytes and fibroblasts. Amplification of c-erbB-1 (EGFR) gene was observed in only one cell line whereas no amplification of other c-erbB ge nes was found. Overexpression of EGFR, c-erbB-2, c-erbB-3 and c-erbB-4 mRNA s was observed in 10, 14, 10 and 8 out of 15 head and neck cell lines respe ctively. Overexpression of c-erbB-3 and c-erbB-4 was more frequently observ ed in newly derived HNSCC lines than in long-established cell lines. The ma jority of tumor cells also expressed multiple c-erbB ligands, One selected cell line, SIHN-006, was shown to exhibit tyrosine phosphorylation via all four receptors. These new cell lines could provide a useful experimental mo del to study the co-operative signaling of type I tyrosine kinase receptors in HNSCC progression.