OBJECTIVE: To investigate the differences in the pattern of glucose transporter (GLUT) gene expression between normal and tumour tissues and among histological subtypes of renal cell carcinomas (RCCs), as malignant cells are characterized by increased glucose uptake and use. MATERIALS AND METHODS: Enhanced glucose uptake probably depends on the overexpression of GLUT, usually GLUT1 and/or GLUT3, but there are few comprehensive studies to evaluate the relative expression pattern and level of GLUT in normal and tumour kidney tissues, especially of the recently identified GLUT genes. In all, 71 kidney surgical samples were evaluated using reverse transcriptase-polymerase chain reaction (RT-PCR) for GLUT1-14 in normal and tumour (clear cell, papillary and chromophobe RCC, and oncocytoma) tissues. The expression levels for GLUT1-5, 9, 10 and 12 were quantified by real-time quantitative PCR. RESULTS: The RT-PCR results showed that normal kidney tissue expresses all the GLUT isoforms. In clear cell RCC GLUT1 expression increased (P<0.001) while GLUT4, 9 and 12 decreased (P<0.001). In papillary RCC there were no significant increases in GLUT expression, with only GLUT12 significantly expressed at lower levels (P<0.001). In chromophobe RCC the expression of GLUT4 increased (P<0.05), and GLUT2 and 5 decreased (P<0.01), whereas in oncocytoma tissue there were no significant changes in the expression of GLUT1 (P<0.01), 2, 5, 9 (P<0.001) and 10 (P<0.05). CONCLUSIONS: These results suggest that high-affinity GLUTs might have a major role in enhanced glucose uptake in kidney tumours, and that histopathological types are characterized by specific patterns of GLUT expression.
OBJECTIVE: To investigate the differences in the pattern of glucose transporter (GLUT) gene expression between normal and tumour tissues and among histological subtypes of renal cell carcinomas (RCCs), as malignant cells are characterized by increased glucose uptake and use. MATERIALS AND METHODS: Enhanced glucose uptake probably depends on the overexpression of GLUT, usually GLUT1 and/or GLUT3, but there are few comprehensive studies to evaluate the relative expression pattern and level of GLUT in normal and tumour kidney tissues, especially of the recently identified GLUT genes. In all, 71 kidney surgical samples were evaluated using reverse transcriptase-polymerase chain reaction (RT-PCR) for GLUT1-14 in normal and tumour (clear cell, papillary and chromophobe RCC, and oncocytoma) tissues. The expression levels for GLUT1-5, 9, 10 and 12 were quantified by real-time quantitative PCR. RESULTS: The RT-PCR results showed that normal kidney tissue expresses all the GLUT isoforms. In clear cell RCC GLUT1 expression increased (P<0.001) while GLUT4, 9 and 12 decreased (P<0.001). In papillary RCC there were no significant increases in GLUT expression, with only GLUT12 significantly expressed at lower levels (P<0.001). In chromophobe RCC the expression of GLUT4 increased (P<0.05), and GLUT2 and 5 decreased (P<0.01), whereas in oncocytoma tissue there were no significant changes in the expression of GLUT1 (P<0.01), 2, 5, 9 (P<0.001) and 10 (P<0.05). CONCLUSIONS: These results suggest that high-affinity GLUTs might have a major role in enhanced glucose uptake in kidney tumours, and that histopathological types are characterized by specific patterns of GLUT expression.
Authors: Denise A Chan; Patrick D Sutphin; Phuong Nguyen; Sandra Turcotte; Edwin W Lai; Alice Banh; Gloria E Reynolds; Jen-Tsan Chi; Jason Wu; David E Solow-Cordero; Muriel Bonnet; Jack U Flanagan; Donna M Bouley; Edward E Graves; William A Denny; Michael P Hay; Amato J Giaccia Journal: Sci Transl Med Date: 2011-08-03 Impact factor: 17.956
Authors: Kátia C Carvalho; Isabela W Cunha; Rafael M Rocha; Fernanda R Ayala; Mariana M Cajaíba; Maria D Begnami; Rafael S Vilela; Geise R Paiva; Rodrigo G Andrade; Fernando A Soares Journal: Clinics (Sao Paulo) Date: 2011 Impact factor: 2.365
Authors: Jonai Pujol-Gimenez; Fátima Pérez de Heredia; Miguel Angel Idoate; Rachel Airley; María Pilar Lostao; Andrew Robert Evans Journal: J Cancer Date: 2015-01-05 Impact factor: 4.207