BACKGROUND/AIMS: Although cancer cells are known to have an increased rate of glucose metabolism, the complete mechanism for increased glucose uptake in tumor cells is unknown. METHODOLOGY: The presence of mRNA for 5 facilitative glucose transporter (GLUT) isoforms was evaluated by reverse transcription-polymerase chain reaction (RT-PCR) in paired samples of normal gastric mucosa and gastric tumor from 20 individuals. Expression of GLUT proteins was immunohistochemically determined in 70 resected gastric cancer specimens. RESULTS: By using RT-PCR, GLUT2 mRNA was detected in 80% of normal gastric mucosal samples, while GLUT4 mRNA was seen in only 40%, GLUT1 mRNA was not detected in normal gastric mucosa. In gastric carcinoma samples, GLUT1 mRNA was detected in 19 out of 20 cases (95%) and GLUT2, GLUT3, and GLUT4 mRNAs in all samples. By immunohistochemistry, GLUT1 protein was detected in 19% of the tumors. A majority of tumors (61%) expressed 1 or more transporter protein. The presence of GLUT1 protein in a tumor was positively correlated with the tumor's invasion into the gastric wall, lymphatics or blood vessels and with lymph node metastases. The post-operative survival of patients with tumor expressing GLUT1 protein was significantly worse than those with tumor without GLUT1 protein. CONCLUSIONS: Gastric cancer cells may acquire the ability to produce GLUT1 mRNA by malignant transformation. Increased expression of the high-affinity glucose transporters, GLUT1 and/or GLUT4, in tumor cells may drain glucose preferentially to the tumor at the expense of the tumor-bearing host.
BACKGROUND/AIMS: Although cancer cells are known to have an increased rate of glucose metabolism, the complete mechanism for increased glucose uptake in tumor cells is unknown. METHODOLOGY: The presence of mRNA for 5 facilitative glucose transporter (GLUT) isoforms was evaluated by reverse transcription-polymerase chain reaction (RT-PCR) in paired samples of normal gastric mucosa and gastric tumor from 20 individuals. Expression of GLUT proteins was immunohistochemically determined in 70 resected gastric cancer specimens. RESULTS: By using RT-PCR, GLUT2 mRNA was detected in 80% of normal gastric mucosal samples, while GLUT4 mRNA was seen in only 40%, GLUT1 mRNA was not detected in normal gastric mucosa. In gastric carcinoma samples, GLUT1 mRNA was detected in 19 out of 20 cases (95%) and GLUT2, GLUT3, and GLUT4 mRNAs in all samples. By immunohistochemistry, GLUT1 protein was detected in 19% of the tumors. A majority of tumors (61%) expressed 1 or more transporter protein. The presence of GLUT1 protein in a tumor was positively correlated with the tumor's invasion into the gastric wall, lymphatics or blood vessels and with lymph node metastases. The post-operative survival of patients with tumor expressing GLUT1 protein was significantly worse than those with tumor without GLUT1 protein. CONCLUSIONS:Gastric cancer cells may acquire the ability to produce GLUT1 mRNA by malignant transformation. Increased expression of the high-affinity glucose transporters, GLUT1 and/or GLUT4, in tumor cells may drain glucose preferentially to the tumor at the expense of the tumor-bearing host.
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