Objective  To explore the effects of CD147/HAb18G genetic engineering monoclonal antibody on the distribution of monocarboxylate transporter-1(MCT1) in U251 cells

and its influence on lactic metabolism of glycolysis.    Methods  U251 glioblastoma cells were divided into control (10

mg/L human IgG 0.5 ml)

low dose (5 mg/L CD147/HAb18G Mab 0.5 ml) and high dose (10 mg/L CD147/HAb18G Mab 0.5 ml) groups. The change of MCT1 expression and distribution in each group were demonstrated by immunofluorescence staining. Intracellular lactic acid content were detected by spectrophotometer

and cell growth curves and data of each group recorded for statistical comparison.    Results  The expression and distribution of MCT1 were significantly changed in low and high dose groups. Compared with control group

valid expression of MCT1 on cell membrane was decreased (random observation of 500 cells for each sample

the cell counts of completed membrane expression in contrast group: 367.34±6.92

low dose group: 161.92±7.33

high dose group: 54.58±4.80

P0.01)

while invalid accumulation of MCT1 in plasma was increased (the cell counts of plasma expression in control group 12.08±3.03

low dose group 70.83±4.71

high dose group 264.58±6.14

P0.01). Intracellular lactic acid content was significantly enhanced (the lactic acid content in contrast group: 0.222±0.020 mmol/L

low dose group: 0.418±0.015 mmol/L

high dose group: 0.713±0.018 mmol/L

P0.01).Growth curves and data also showed difference among 3 groups [the mean max cell density in control group: (5.24±0.37)×10

5

/ml

low dose group: (4.23±0.48)×10

5

/ml

high dose group: (3.19±0.46)×10

5

/ml

P0.01

]

. The variations mentioned above also had statistical difference between low and high dose group (P0.05).    Conclusion   CD147/HAb18G monoclonal antibody reduces valid expression of MCT1 on cell membrane by interfering CD147 guiding interactions with MCT1

and restrains the drainage of intracellular lactic acid generated by glycolysis. It has suppression on tumor cell growth.