1.Effect of pterostilbene on apoptosis and glycolysis of ovarian cancer SKOV3 cells and its mechanism
Li HUANG ; Youmei LONG ; Yixia FU ; Liangbin XIA
Practical Oncology Journal 2019;33(6):502-507
Objective The aim of this study was to investigate the effect and mechanism of pterostilbene on apoptosis and glycolysis of ovarian cancer SKOV3 cells. Methods SKOV3 cells were treated with 0,25,50,100 and 150 μmol/L of pterostilbene for 24,48 and 72 hours. The proliferation of SKOV3 cells was measured by CCK. The effect of pterostilbene on apoptosis of SKOV3 cells was determined by flow cytometry. The glucose consumption and lactate production were detected by glucose oxidase assay and chemical colorimetry. The expression of signal transducer and activator of transcription 3 ( STAT3 ), phosphorylated STAT3 ( p -STAT3) and hexokinase 2 ( HK2) proteins was detected by Western blot. The expression of glucose transporter 1 ( GLUT1) and M2 pyruvate kinase(PKM2)mRNA was detected by qRT-PCR. Results Pterostilbene inhibited the proliferation of SKOV3 cells in a time- and dose-dependent manner. According to CCK-8 results,100 μmol/L of pterostilbene was selected as the follow-up ex-perimental group and 0 μmol/L as a control group. Pterostilbene could significantly promote the apoptosis of SKOV3 cells in a dose-dependent manner. The higher the concentration,the more obvious apoptosis effect,the difference was statistically significant ( P <0. 05). In addition,the levels of glucose consumption and lactate production in the 100 μmol/L group were significantly lower than those in the 0 μmol/L group(P<0. 01). The expression of p-STAT3 and HK2 protein in the 100 μmol/L group was also significant-ly lower than those in the 0 μmol/L group(P<0. 001). The expression of GLUT1and PKM2 mRNA in the 100 μmol/L group was also significantly decreased than those in the 0 μmol/L group(P<0. 01). Conclusion Pterostilbene can inhibit the proliferation of SK-OV3 cells and promote apoptosis,and may inhibit the glycolysis of ovarian cancer through a STAT3/HK2 pathway.