Coregulation of glucose uptake and vascular endothelial growth factor (VEGF) in two small-cell lung cancer (SCLC) sublines in vivo and in vitro
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Coregulation of glucose uptake and vascular endothelial growth factor (VEGF) in two small-cell lung cancer (SCLC) sublines in vivo and in vitro. / Pedersen, M W; Holm, S; Lund, E L; Højgaard, L; Kristjansen, P E.
In: Neoplasia (New York, N.Y.), Vol. 3, No. 1, 28.04.2001, p. 80-7.Research output: Contribution to journal › Journal article › Research › peer-review
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TY - JOUR
T1 - Coregulation of glucose uptake and vascular endothelial growth factor (VEGF) in two small-cell lung cancer (SCLC) sublines in vivo and in vitro
AU - Pedersen, M W
AU - Holm, S
AU - Lund, E L
AU - Højgaard, L
AU - Kristjansen, P E
PY - 2001/4/28
Y1 - 2001/4/28
N2 - We examined the relationship between (18)F- labeled 2-fluro-2-deoxy-d-glucose (FDG) uptake, and expression of glucose transporters (GLUTs) in two human small-cell lung cancer (SCLC) lines CPH 54A and CPH 54B. Changes in the expression of GLUTs and vascular endothelial growth factor (VEGF) during 12-, 18-, and 24 hours of severe hypoxia in vivo (xenografts) and in vitro (cell cultures) were recorded for both tumor lines. The two SCLC lines are subpopulations of the same patient tumor. In spite of their common genomic origin they represent consistently different metabolic and microenvironmental phenotypes as well as treatment sensitivities. There were higher levels of Glut-1 protein in 54B and a correspondingly higher FDG uptake in this tumor line (P<.001). During hypoxia a significant upregulation of in VEGF mRNA, GLUT-1 mRNA, and Glut-1 and -3 protein occurred with a distinctly different time course in the two cell lines. A similar co-upregulation of GLUT and VEGF was seen in hypoxic tumors of both lines. There were no significant changes of HIF-1alpha mRNA during hypoxia in either of the cell lines. A more detailed understanding of such correlations between glucose metabolism, angiogenesis, and microenvironmental phenotype of tumors, by positron emission tomography (PET) and molecular techniques might further sophisticate our interpretation of glycolytic predominance in tumors as seen by 18FFDG PET.
AB - We examined the relationship between (18)F- labeled 2-fluro-2-deoxy-d-glucose (FDG) uptake, and expression of glucose transporters (GLUTs) in two human small-cell lung cancer (SCLC) lines CPH 54A and CPH 54B. Changes in the expression of GLUTs and vascular endothelial growth factor (VEGF) during 12-, 18-, and 24 hours of severe hypoxia in vivo (xenografts) and in vitro (cell cultures) were recorded for both tumor lines. The two SCLC lines are subpopulations of the same patient tumor. In spite of their common genomic origin they represent consistently different metabolic and microenvironmental phenotypes as well as treatment sensitivities. There were higher levels of Glut-1 protein in 54B and a correspondingly higher FDG uptake in this tumor line (P<.001). During hypoxia a significant upregulation of in VEGF mRNA, GLUT-1 mRNA, and Glut-1 and -3 protein occurred with a distinctly different time course in the two cell lines. A similar co-upregulation of GLUT and VEGF was seen in hypoxic tumors of both lines. There were no significant changes of HIF-1alpha mRNA during hypoxia in either of the cell lines. A more detailed understanding of such correlations between glucose metabolism, angiogenesis, and microenvironmental phenotype of tumors, by positron emission tomography (PET) and molecular techniques might further sophisticate our interpretation of glycolytic predominance in tumors as seen by 18FFDG PET.
KW - Animals
KW - Anoxia
KW - Blotting, Western
KW - Carcinoma, Small Cell
KW - DNA-Binding Proteins
KW - Endothelial Growth Factors
KW - Fluorodeoxyglucose F18
KW - Glucose
KW - Glucose Transporter Type 1
KW - Humans
KW - Hypoxia-Inducible Factor 1
KW - Hypoxia-Inducible Factor 1, alpha Subunit
KW - In Vitro Techniques
KW - Lung Neoplasms
KW - Lymphokines
KW - Male
KW - Mice
KW - Mice, Nude
KW - Monosaccharide Transport Proteins
KW - Nuclear Proteins
KW - RNA, Messenger
KW - Tomography, Emission-Computed
KW - Transcription Factors
KW - Tumor Cells, Cultured
KW - Up-Regulation
KW - Vascular Endothelial Growth Factor A
KW - Vascular Endothelial Growth Factors
KW - Journal Article
KW - Research Support, Non-U.S. Gov't
U2 - 10.1038/sj/neo/7900133
DO - 10.1038/sj/neo/7900133
M3 - Journal article
C2 - 11326319
VL - 3
SP - 80
EP - 87
JO - Neoplasia
JF - Neoplasia
SN - 1522-8002
IS - 1
ER -
ID: 165883329