Abstract
We attempted to suppress glucose transporter 1 (GLUT1) expression by transfecting MKN45 cells with cDNA for antisense GLUT1. Glucose transport was significantly decreased in cells with antisense GLUT1 compared with wild-type cells or cells with vector alone. Suppression of GLUT1 mRNA resulted in a decreased number of cells in the S phase. This was accompanied by overexpression of p21 protein. Tumorigenicity in the nude mice injected with antisense GLUT1 expressing cells was significantly slower than in those with wild-type MKN45 cells. These results suggest that antisense GLUT1 mRNA inhibits tumor growth through a G(1) arrest and that expression of antisense GLUT1 mRNA via gene therapy can be used as a tool in the treatment of cancer.
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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Animals
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Apoptosis
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Biological Transport / genetics
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DNA Fragmentation
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DNA, Antisense / metabolism
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DNA, Complementary / metabolism
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Dose-Response Relationship, Drug
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Flow Cytometry
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G1 Phase
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Glucose Transporter Type 1
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Kinetics
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Mice
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Mice, Inbred ICR
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Mice, Nude
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Monosaccharide Transport Proteins / genetics*
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Monosaccharide Transport Proteins / metabolism*
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Neoplasm Transplantation
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Neoplasms, Experimental / pathology*
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Proto-Oncogene Proteins p21(ras) / biosynthesis
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RNA, Messenger / metabolism
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Reverse Transcriptase Polymerase Chain Reaction
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S Phase
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Stomach Neoplasms / metabolism
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Suppression, Genetic
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Time Factors
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Transfection
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Tumor Cells, Cultured
Substances
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DNA, Antisense
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DNA, Complementary
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Glucose Transporter Type 1
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Monosaccharide Transport Proteins
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RNA, Messenger
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Slc2a1 protein, mouse
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Proto-Oncogene Proteins p21(ras)