Mechanisms related to [F-18]fluorodeoxyglucose uptake of human colon cancers transplanted in nude mice

[F-18]Fluorodeoxyglucose ([F-18]FDG), a glucose analogue, has been widely u sed for tumor imaging. To investigate the mechanisms related to [F-18]FDG u ptake by tumors, an experiment involving nude mice was performed. Methods: Human colon cancer cell lines SNU-C2A, SNU-C4 and SNU-C5 were transplanted to nude mice. Using immunohistochemical staining and Western blot, the expr ession of glucose transporter (Glut) isoforms (Glut-1 similar to 5) in xeno grafted tumors was analyzed. For the analysis of messenger ribonucleic acid (mRNA) expression, reverse-transcription polymerase chain reaction and Nor thern blot were used and the enzyme activity of hexokinase in cancer tissue s was measured by continuous spectrophotometric rate determination. Results : [F-18]FDG uptake in SNU-C4 and SNU-C5 cells was higher than in normal col on cells. Among these cells and xenografted tumors, SNU-C5 showed the highe st level of [F-18]FDG uptake, followed by SNU-C4 and SNU-C2A. An immunostai ning experiment showed intense staining of Glut-1 in SNU-C5 tumors but some what faint staining in SNU-C4. SNU-C5 tumors also showed positive staining with Glut-3, although this was not the case with SNU-C2A and SNU-C4. Wester n blot analysis showed the expression of Glut-1 and Glut-3 in all tumors. E xperiments involving Northern blot analysis and reverse-transcription polym erase chain reaction confirmed the overexpression of Glut-1 mRNA in all tum ors, with the highest level in SNU-C5. The level of Glut-3 mRNA was also el evated in SNU-C5 tumors but not in SNU-C2A and SNU-C4. The enzyme activity of hexokinase did not vary among different tumors. Conclusion: Gluts, espec ially Glut-1, are responsible for [F-18]FDG uptake in a nude mouse model of colon cancer rather than hexokinase activity. Increased numbers of glucose transporters at the plasma membrane of cancer cells is attributed to an in creased level of transcripts of glucose transporter genes and may be a caus e of increased [F-18]FDG uptake, at least in colon cancer tumors.