Àá½Ã¸¸ ±â´Ù·Á ÁÖ¼¼¿ä. ·ÎµùÁßÀÔ´Ï´Ù.

±¸°­¾Ï ¼¼Æ÷ÁÖÀÇ c-Ki-ras 2 À¯ÀüÀÚ ¹ßÇö ¹× Á¡µ¹¿¬º¯ÀÌ¿¡ °üÇÑ ¿¬±¸

c-Ki-ras 2 gene expression and point mutation in human oral cancer

´ëÇѱ¸°­¾Ç¾È¸é¿Ü°úÇÐȸÁö 1994³â 20±Ç 3È£ p.265 ~ 272
ÀÌÀÇ¿õ,
¼Ò¼Ó »ó¼¼Á¤º¸
ÀÌÀÇ¿õ (  ) - ¿¬¼¼´ëÇб³

Abstract


Five oral cancer cell lines, FaDu, HEp-2 SCC-4, 1483, OEC-M1, and one epidermoid carcinoma cell line, A-431, were examined for their expression level of c-Ki-ras 2 gene and the presence of activating mutations. Northern blot analysis revealed
that
the
expression level of c-Ki-ras 2 mRNA of FaDu cells was 4 times that of primary cultured normal human oral keratinocytes (NHOK).
OEC-M1 cells expressed mRNA of a little smaller size than normal and the expression level was much higher than in NHOK. Other cells expressed c-Ki-ras 2 mRNA at comparable levels to NHOK. DNA sequencing of c-Ki-ras 2 gene exon 1 and exon 2 was
performed
using polymerase chain reactionamplified DNA fragments. OEC-M1 cells had three point mutations in their c-Ki-ras 2 gene exon 1 and exon 2 resulting in amino acid substitutions, asparagine to aspartic acid, phenylalanine to leucine, and glycine to
arginine at 24the , 28th and 53rd residues respectively. However, other cells had no mutation in their c-Ki-ras 2 gene exon 1 and exon 2. This result shows that abberant expression of c-ki-ras 2 gene and the point mutations are quite often
associated
with oral cancer.

Å°¿öµå

¿ø¹® ¹× ¸µÅ©¾Æ¿ô Á¤º¸

  

µîÀçÀú³Î Á¤º¸

KCI
KoreaMed