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目的:确定前列腺癌中Sp1通过PKM2途径对前列腺癌细胞的增殖和代谢的作用。方法:前列腺癌细胞株DU145与PC3体外转染Sp1 si RNA与阴性对照无意义核苷酸序列(NC组),采用葡萄糖检测试剂盒与乳酸检测试剂盒检测转染后有氧糖酵解变化;CCK-8实验检测转染后的细胞增殖;q RT-PCR检测转染后PKM2表达;Western Blotting检测转染后Sp1与PKM2表达。结果:DU145与PC3转染Sp1 si RNA后与NC组比较,剩余葡萄糖显著偏高,乳酸产生显著下降;CCK8实验表明抑制Sp1后能显著抑制前列腺癌细胞的增殖能力;q RT-PCR实验显示抑制Sp1后明显抑制PKM2的表达;Western Blotting显示转染的Sp1 si RNA对Sp1具有较高的沉默效率,且PKM2的表达也降低。结论:Sp1在前列腺癌细胞株DU145与PC3中可通过直接作用于PKM2促进细胞代谢。
PURPOSE: To determine the effect of Sp1 on the proliferation and metabolism of prostate cancer cells through the PKM2 pathway in prostate cancer. METHODS: The prostate cancer cell lines DU145 and PC3 were transfected with Sp1 si RNA and negative control non-sense nucleotide sequences (NC group) in vitro. The changes of aerobic glycolysis after transfection were detected by glucose detection kit and lactic acid detection kit. The cell proliferation was detected by CCK-8 assay. The expression of PKM2 was detected by q RT-PCR. The expression of Sp1 and PKM2 was detected by Western Blotting. Results: Compared with NC group, DU145 and PC3 transfected Sp1 si RNA showed significantly higher residual glucose and decreased lactate production; CCK8 assay showed that inhibition of Sp1 significantly inhibited the proliferation of prostate cancer cells; q RT-PCR showed that inhibition Sp1 significantly inhibited the expression of PKM2; Western Blotting showed that transfected Sp1 si RNA had higher silencing efficiency on Sp1 and PKM2 expression was also decreased. Conclusion: Sp1 promotes cell metabolism by directly acting on PKM2 in prostate cancer cell lines DU145 and PC3.