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Background:The clinicopathological parameters associated with glucose transporter-1 (GLUT-1) expression in advanced gastric cancer are still controversial. This study aimed to determine the clinicopathological parameters and prognosis associated with GLUT-1 expression in advanced gastric cancer. Material/Methods:The GLUT-1 expression level of 234 consecutive gastric cancer samples was detected by immunohistochemical staining and evaluated by semiquantitative analysis. The clinicopathological data and expression level of GLUT-1 of enrolled patients were retrospectively analyzed with univariate and multivariate analyses. Results:Tumor size, depth of invasion, and Lauren classification were independent factors related to GLUT-1 expression (P<0.05). Within advanced gastric cancer, tumor size and Lauren type were independent factors associated with GLUT-1 (P=0.011, P<0.001, respectively). The mean survival time of GLUT-1-positive patients with stage M0 advanced gastric cancer who had undergone radical gastrectomy was shorter than that of GLUT-1negative patients (61.26±6.12 versus 80.88±7.38, P=0.044). GLUT-1 was an independent prognosis factor in locally advanced gastric cancer patients who had undergone radical gastrectomy (hazard ratio [HR] 1.769, P=0.046). The mean survival time of adjuvant chemotherapy was significantly better than no adjuvant chemotherapy in the GLUT-1-positive group (71.10±6.88 versus 24.65±8.69, P<0.001) and in the GLUT-1 negative group (87.48±7.99 versus 49.39±11.71, P<0.001). Conclusions:Tumor size and Lauren type independently affected GLUT-1 expression in advanced gastric cancer. GLUT-1 was not only related to poor prognosis but also predicted to be a metabolic biomarker for intestinal type in locally advanced gastric cancer. The relationship among GLUT-1, hepatic metastasis and chemotherapy regimens, and mechanism of chemotherapy responses related to GLUT-1 should be further investigated.

The effect of hyperthermic carbon dioxide (CO2) pneumoperitoneum in combination with 5-fluorouracil (5-FU) on the proliferation and invasion of colon cancer was explored. Colon cancer cell line SW-480 was sealed into the urine collection bag to simulate pneumoperitoneum with 100% CO2 under a pressure of 12 mmHg. The cells were divided into group A, CO2 at 37˚C; group B, CO2 at 43˚C; group C, 5-FU; group D, CO2 at 37˚C+5-FU; group E, CO2 at 43˚C+5-FU; and control groups under normal culture conditions. The cell proliferation was assessed by CCK-8 test; the cell apoptosis was tested by FACS analysis; the cell invasion was examined by Transwell assay; the expression of HSP-70, caspase-3, HIF-1α and MMP-9 proteins and genes were detected by western blot analysis and RT-PCR. The SW-480 cells were injected into nude mouse cecum subserosal to establish a colon cancer model. We applied 43˚C CO2 pneumoperitoneum or 5-FU intraperitoneal chemotherapy to intervene, detected the transplantation tumor growth and metastasis. The cell proliferation was inhibited in groups B, C, D and E, apoptosis was induced in groups B, C, D and E, the Transwell cell number decreased in groups B, C, D and E, the transplantation tumor weight and metastasis rate were inhibited in groups B, C, D and E, but all not in group A. The most significant change was observed in group E. Hyperthermic CO2 pneumoperitoneum was able to reinforce the inhibition of 5-FU on proliferation and invasion of colon cancer.

Abstract. The present study explored the inhibitory effect of hyperthermic CO 2 pneumoperitoneum on the proliferation and migration of colon cancer cells, and its mechanism. Colon cancer cell line SW-480 was sealed into a urine collection bag to simulate pneumoperitoneum with 100% CO 2 under a pressure of 14 mmHg. The growth and morphology of cells were observed under a microscope, the inhibition on cell proliferation was measured using WST-8 test, cell apoptosis and the cell cycle were monitored using fluorescence-activated cell sorting analysis, the migration of cells was tested using the scratch assay, and the expression of HSP-70, caspase-3, hypoxiainducible factor-1α and matrix metalloproteinase-9 (MMP-9) proteins and genes was investigated using western blotting and reverse transcription polymerase chain reaction. Compared with the control group, there was no significant difference in the CO 2 group (P>0.05), while the apoptosis and necrosis rates in the hyperthermo-CO 2 group was significantly increased (P<0.05). Compared with the control group, the number of cells at G0/G1 phase significantly increased and the number of cells at S phase significantly decreased in the hyperthermo-CO 2 group (P<0.05), indicating that hyperthermo-CO 2 could arrest the cell cycle. It was suggested by the results of the scratch assay that cell migration ability enhanced in the CO 2 group, but decreased in the hyperthermo-CO 2 group compared with the control. CO 2 pneumoperitoneum promoted cell migration by upregulating HIF-1α and MMP-9 expression. However, the CO 2 pneumoperitoneum with hyperthermia enhanced apoptosis and inhibited migration by upregulating the expression of HSP-70, HIF-1α and caspase-3, but downregulating the expression of MMP-9.