AIM:To investigate the possible mechanism of how glucose promotes invasion and metastasis of colon cancer cells.METHODS:CT-26 rat colorectal cancer cells were cultured in different concentrations of glucose environments(10,20,and 30 mmol/L).Wound healing assay and transwell chamber invasion assay were utilized to test the migration and invasion,respectively.In order to understand the role of signal transducer and activator of transcription 3(STAT3)in the process,STAT3 inhibitors,including Stattic(an STAT3 specific inhibitor)and small interfering RNA targeting STAT3,were used to block STAT3 function to evaluate their impact on CT-26 cell motion.To verify whether STAT3 and matrix metalloproteinase-9(MMP-9)protein expression is associated with glucose-induced cell movement,Western blot was used to compare the differences in the expression of MMP-9 and STAT3 in cells incubated with and without STAT3 inhibitors in high glucose condition.RESULTS:In both wound healing and invasion assays,the migration and invasion of CT-26 cells increased gradually with the increase in glucose concentration.However,the glucose-induced migration and invasion were obviously inhibited by STAT3 inhibitors(P<0.05).Similarly,in Western blot assessment,both MMP-9and STAT3 expression increased under a high glucose environment and the highest expression was achieved when 30 mmol/L glucose was used.However,in cells treated with 30 mmol/L mannitol,either MMP-9 or STAT3expression did not increase(P>0.05).When STAT3inhibitors were added in the 30 m M glucose group,not only STAT3 but also MMP-9 expression decreased significantly(P<0.05).CONCLUSION:Our study provides evidence that glucose can promote both migration and invasion of CT-26 cells,and that the STAT3-induced MMP-9 signal pathway is involved in this process. AIM: To investigate the possible mechanism of how glucose promotes invasion and metastasis of colon cancer cells. METHODS: CT-26 rat colorectal cancer cells were cultured in different concentrations of glucose environments (10, 20, and 30 mmol / L) assay and transwell chamber invasion assay were utilized to test the migration and invasion, respectively. In order to understand the role of signal transducer and activator of transcription 3 (STAT3) in the process, STAT3 inhibitors, including Stattic (an STAT3 specific inhibitor) and Small interfering RNA targeting STAT3, were used to block STAT3 function to evaluate their impact on CT-26 cell motion. To verify whether STAT3 and matrix metalloproteinase-9 (MMP-9) protein expression is associated with glucose-induced cell movement, Western blot was used to compare the differences in the expression of MMP-9 and STAT3 in cells incubated with and without STAT3 inhibitors in high glucose condition .RESULTS: In both wound healing and invasive assays, the The migration and invasion of CT-26 cells increased gradually with the increase in glucose concentration. However, the glucose-induced migration and invasion were obviously inhibited by STAT3 inhibitors (P <0.05). Similarity, in Western blot assessment, both MMP-9 and STAT3 expression increased under a high glucose environment and the highest expression was achieved when 30 mmol / L glucose was used. Host, in cells treated with 30 mmol / L mannitol, either MMP-9 or STAT3 expression did not increase (P> 0.05) STAT3 inhibitors were added in the 30 m M glucose group, not only STAT3 but also MMP-9 expression decreased significantly (P <0.05) .CONCLUSION: Our study provides evidence that glucose can promote both migration and invasion of CT-26 cells, and that the STAT3-induced MMP-9 signal pathway is involved in this process.