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As one of the causes of exercise-induced fatigue, exercise-induced metabolic acidosis has attracted much attention. The effect of pyruvate supplementation on exercise-induced metabolic acidosis is rarely reported, and its mechanism has not been fully elucidated. Monocarboxylate transporters (MCTs) play an important role in the maintenance of the acid-base balance, but it is not clear whether pyruvate can alleviate acidosis by increasing the expression of MCTs. In this study, pyruvate (616 mg/kg/day) was supplemented to rats for one week, and then acute HIIE was performed. The HIIE protocol comprised 13 repeats of a 60 s sprint session at 110% VO
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@#[Abstract] Objective: To investigate the effects of silencing monocarboxylate transporter 4 (MCT4) on the proliferation, migration and invasion of prostate cancer PC3 cells and its possible molecular mechanism. Methods: RNA interference technology was used to transfect siRNA-MCT4 (si-MCT4) and negative control plasmid (si-NC) into PC3 cells, respectively. The content of lactic acid in the cell culture medium of transfected PC3 cells was detected by lactic acid assay after culturing for 96 h. The proliferation, migration and invasion ability of PC3 cells were detected by CCK-8 and Transwell assay, respectively. Western blotting was used to detect the silencing effect and the expressions of integrin β 4-FAK-SRC-MEK-ERK signaling pathway associated proteins (integrin β4, p-FAK, p-SRC, p-ERK1/2, p-MEK1/2) and EMT associated proteins (E-cadherin and N-cadherin). Results: PC3 cell line with silenced MCT4 was successfully constructed. Compared with the control group, the content of extracellular lactic acid in the PC3 cell culture medium of the si-MCT4 group was significantly decreased (P<0.01), and the proliferation, migration and invasion of cells were significantly decreased (P<0.05 or P<0.01). Compared with the control group, the protein expressions of integrin β4, p-FAK, p-SRC, p-MEK1/2, p-ERK1/2 and N-cadherin were significantly decreased (all P<0.01), while the protein expression of E-cadherin was significantly increased (P<0.01). Conclusion: Silencing MCT4 can significantly inhibit the proliferation, migration and invasion of PC3 cells, the mechanism of which may be related to the inhibition of lactic acid level in cell culture medium and suppression of integrin β4-FAK-SRC-MEKERK signaling pathway associated proteins as well as EMT associated proteins.
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Objective To investigate the correlation between the expression of glucose transporters 1 (GLUT1),monocarboxylate transporter 1 (MCT1),monocarboxylate transporter 4(MCT4) and clinical characteristics in colon cancer. Methods From January 2008 to January 2016,the carcinoma tissues of 84 cases with colon cancer after gastrointestinal surgery, and 40 samples of corresponding adjacent normal colon tissues in the First People＇s Hospital of Hangzhou were collected. The clinical data were collected. Immunohistochemistry was performed to detect the expression of GLUT1, MCT1 and MCT4, the results were analyzed. Results The positive expression rates of MCT1,GLUT1 and MCT4 in colon cancer were 54. 8% (46/84),47. 6% (40/84),58. 3% (49/84),respectively, which were significantly higher than those of the control group[12. 5% (5/40),7. 5% (3/40),15. 0% (6/40)],the differences were statistically significant (χ2=19. 987,19. 253,20. 615,all P＜0. 01). The expressions of GLUT1, MCT1,and MCT4 were not related to gender,age and tumor size,but related to lesion location,differentiation,lymph node metastasis,distant metastasis and clinical stage( GLUT1:χ2=6. 227,11. 629,10. 029,14. 817,4. 709;MCT1:χ2=6. 891,8. 615,9. 185,5. 337,16. 131;MCT4:χ2=8. 641,7. 077,12. 131,6. 917,7. 077;all P ＜0. 05). Conclusion High expression of GLUT1,MCT1 and MCT4 were observed in colon cancer. GLUT1,MCT1 and MCT4 may affect the development of colon cancer through energy metabolism pathway in colon cancer tissues.
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PURPOSE: The aim of this study was to assess the expression of metabolism-related proteins including glucose transporter 1 (Glut-1), carbonic anhydrase IX (CAIX) and monocarboxylate transporter 4 (MCT4) in breast mucinous carcinoma and to evaluate the implications of the results. METHODS: Immunohistochemical staining for Glut-1, CAIX, and MCT4 was performed on tissue sections from 59 cases of mucinous carcinoma to evaluate the association between the expression of metabolism-related proteins and clinicopathologic factors. Mucinous carcinoma was subclassified into type A and type B according to histopathological characteristics. RESULTS: Of the 59 patients, 35 patients (59.3%) were type A mucinous carcinoma and 24 patients (40.7%) were type B mucinous carcinoma. Stromal expression of MCT4 was significantly associated with a high histologic grade (p=0.022) and type B mucinous carcinoma (p=0.016). There were significant positive correlations between the expression of Glut-1, CAIX and tumoral expression of MCT4 (p<0.05). CONCLUSION: We assessed the expression of metabolism-related proteins including Glut-1, CAIX, and MCT4 in breast mucinous carcinoma and found that the stromal expression of MCT4 was higher in type B mucinous carcinoma than in type A, which reflected a difference in the tumor microenvironment.