Antisense epidermal growth factor receptor (EGFR) transfection down-regulates EGFR expression and suppresses the malignant phenotype of human nasopharyngeal carcinoma CNE-2 cell line.

OBJECTIVE

To determine whether epidermal growth factor receptor (EGFR) expression contributes to tumor growth of poorly differentiated human nasopharyngeal carcinoma CNE-2 cell lines.

METHODS

An expression vector containing a N-terminal fragment (1.35 kb) of human EGFR in the antisense orientation was transfected into CNE-2 cell lines via lipofectamine. The established clones resistant to G418 were isolated and characterized, and the tumor-inhibiting effect of antisense EGFR expression was evaluated in terms of tumor growth and metastasis at different time after subcutaneous inoculation into nude mice.

RESULTS

Down-regulated EGFR expression in the cells with antisense vector transfection was demonstrated by ligand binding assay. The growth rate and the ability to grow in soft agarose of these antisense transfectants were also reduced. After inoculation into nude mice, EGFR antisense transfectants showed a longer latency period, slower tumor growth and lower metastatic rates to the lymph nodes and lung in comparison with the parental cells.

CONCLUSIONS

These results suggest that these EGFR antisense cDNA-transfected CNE-2 cells are of value to further delineate the role of EGFR in the development and progression of nasopharyngeal carcinoma.