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.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Adenocarcinoma / metabolism*
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Colon / metabolism
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Colonic Neoplasms / metabolism*
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Gene Expression Regulation, Neoplastic*
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Genes, ras / genetics*
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Glucose Transporter Type 1
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Glucose Transporter Type 2
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Glucose Transporter Type 3
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Glucose Transporter Type 4
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Glucose Transporter Type 5
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Humans
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Monosaccharide Transport Proteins / genetics
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Monosaccharide Transport Proteins / metabolism*
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Mucous Membrane / metabolism
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Muscle Proteins*
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Nerve Tissue Proteins*
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Point Mutation
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RNA, Messenger / metabolism
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Reverse Transcriptase Polymerase Chain Reaction
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ras Proteins / metabolism*
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ras Proteins / physiology
Substances
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Glucose Transporter Type 1
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Glucose Transporter Type 2
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Glucose Transporter Type 3
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Glucose Transporter Type 4
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Glucose Transporter Type 5
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Monosaccharide Transport Proteins
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Muscle Proteins
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Nerve Tissue Proteins
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RNA, Messenger
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SLC2A1 protein, human
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SLC2A3 protein, human
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SLC2A4 protein, human
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ras Proteins