目的：探讨沉默单羧酸转运体4（monocarboxylate transporter 4，MCT4）对前列腺癌PC3细胞增殖、迁移和侵袭的影响 及其可能的分子机制。方法：利用RNA干扰技术分别将siRNA-MCT4（si-MCT4）和阴性对照质粒（si-NC）转染进PC3细胞，培养 96 h后用乳酸测定法检测转染后PC3细胞培养液中乳酸含量， 用CCK-8法、Transwell小室法分别检测PC3细胞的增殖、迁移和侵 袭能力， 用Western blotting检测沉默效果及细胞中 integrin β4-FAK-SRC-MEK-ERK 信号通路相关蛋白（integrin β4、p-FAK、 p-SRC、p-ERK1/2、p-MEK1/2）和EMT相关蛋白（E-cadherin、N-cadherin）的表达水平。结果：成功构建沉默MCT4的PC3细胞株。 与对照组比较，si-MCT4组PC3细胞培养液中乳酸含量显著降低（P<0.01)，细胞的增殖、迁移和侵袭能力均显著降低（P<0.05或 P<0.01）；si-MCT4组PC3细胞中integrin β4、p-FAK、p-SRC、p-ERK1/2、p-MEK1/2 及 N-cadherin 水平显著降低（均 P<0.01）， 而 E-cadherin表达水平显著升高（P<0.01）。结论：沉默MCT4表达可显著抑制前列腺癌PC3细胞的增殖、迁移和侵袭能力，其机制 可能与抑制细胞培养液中的乳酸水平和细胞中integrin β4-FAK-SRC-MEK-ERK信号通路及EMT相关蛋白的表达有关。

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 abilityofPC3cellsweredetectedbyCCK-8andTranswellassay,respectively. Western blotting was used to detect the silencing effect and the expressions of integrin β4-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.