Author/Authors :
Noguchi، نويسنده , , Yoshikazu and Okamoto، نويسنده , , Takahide and Marat، نويسنده , , Doulet and Yoshikawa، نويسنده , , Takaki and Saitoh، نويسنده , , Aya and Doi، نويسنده , , Chiharu and Fukuzawa، نويسنده , , Kuniyasu and Tsuburaya، نويسنده , , Akira and Satoh، نويسنده , , Shinobu and Ito، نويسنده , , Takaaki، نويسنده ,
Abstract :
The expression of facilitative glucose transporter isoforms in colon adenocarcinoma and the possible role of k-ras in inducing GLUT (glucose transporter) mRNA were studied. RT-PCR demonstrated GLUT2 and GLUT3 expression in 100% of the ten normal colon mucosa samples but detected no GLUT1 mRNA. By contrast, GLUT1 mRNA was detected in all 20 (100%) colon cancer samples examined. GLUT4 mRNA was not detected in either normal mucosa or colon cancer tissues. Semiquantitative PCR demonstrated equal amounts of GLUT2 and GLUT3 mRNA in both normal mucosa and colon cancer samples. A point mutation in codon 12 of k-ras was detected in only six of the 20 (30%) colon cancer samples. Thus, a major difference between normal colon epithelia and colon cancer was the acquisition of GLUT1 expression, which was unlikely to have been induced by a point mutation in codon 12 of k-ras.
Keywords :
Facilitative glucose transporters , Quantitative competitive PCR , Mutant allele-specific amplification , K-ras
