[MCT4 reduces glucose metabolism and promotes apoptosis of prostate cancer cells].

OBJECTIVE

To investigate the effect of monocarboxylate transporter 4 (MCT4) on the apoptosis and glucose metabolism of prostate cancer cells.

METHODS

We constructed an adenoviral vector containing shRNA-MCT4 and transfected it into the adenocarcinoma cell lines DU145 and PC-3, using the untransfected vector as the blank control and the negative vector as the negative control (shRNA-NC). We determined the MCT4 expression, lactic acid secretion, glucose consumption and apoptosis rate in different groups of cells.

RESULTS

After transfection, the expression of MCT4 in the DU145 and PC-3 cells was significantly lower in the shRNA-MCT4 than in the blank control (P = 0.008 and 0.008) and shRNA-NC groups (P = 0.007 and 0.009), and so were the secretion of lactic acid (P = 0.009 and 0.009; P = 0.009 and 0.008) and single-cell glucose consumption (P = 0.007 and 0.007; P = 0.009 and 0.007). The apoptosis rate of the DU145 cells was remarkably higher in the shRNA-MCT4 than in the blank control and shRNA-NC groups (［22.11 ± 2.68］% vs ［9.81 ± 1.24］% and ［10.01 ± 1.46］%, P = 0.003 and 0.003), and so was that of the PC-3 cells (［23.38 ± 3.08］% vs ［10.21 ± 1.58］% and ［10.91 ± 1.63］%, P = 0.004 and 0.004).

CONCLUSIONS

Inhibiting the expression of MCT4 can interfere with the glucose metabolism and promote the apoptosis of prostate cancer cells. The MCT4 gene is a potential therapeutic target for the treatment of prostate cancer.