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卵泡刺激素促进丙酮酸激酶同工酶 M2 诱导的卵巢癌细胞糖酵解和增殖。

Follicle-stimulating hormone promoted pyruvate kinase isozyme type M2-induced glycolysis and proliferation of ovarian cancer cells.

机构信息

Department of Gynecologic Oncology, Shanghai First Maternity and Infant Hospital, Tongji University School of Medicine, Shanghai, China.

Department of Obstetrics and Gynecology, Shanghai General Hospital, Shanghai Jiaotong University, 100 Haining Road, Shanghai, China.

出版信息

Arch Gynecol Obstet. 2019 May;299(5):1443-1451. doi: 10.1007/s00404-019-05100-4. Epub 2019 Feb 26.

DOI:10.1007/s00404-019-05100-4
PMID:30809696
Abstract

PURPOSE

Reprogramming of cell metabolism is essential for tumor progression and the best-studied metabolic phenomenon of cancer cells is aerobic glycolysis, in which pyruvate kinase isozyme type M2 (PKM2) plays a critical role. Follicle-stimulating hormone (FSH) contributes to epithelial ovarian cancer progression and has been shown to regulate cell metabolism in ovaries. The aim of this study was to investigate the interaction between FSH and PKM2 and their effect on aerobic glycolysis and cell proliferation in ovarian cancer.

METHODS

SKOV3 and OVCAR3 ovarian cancer cells were treated with FSH at various doses to investigate its effect on cell proliferation and PKM2 expression. siRNA-PKM2-transfected SKOV3 and OVCAR3 cells were treated with FSH to examine whether the changes induced by FSH could be altered by siRNA-PKM2. Glucose and lactate levels were evaluated to observe the change in glycolysis in these cells.

RESULTS

In the current study, FSH upregulated the expression of PKM2 and glycolysis in SKOV3 and OVCAR3 cells. PKM2 knockdown reduced FSH-induced cell growth and glycolysis. Moreover, FSH attenuated apoptosis that was induced by the inhibition of PKM2.

CONCLUSIONS

Collectively, the findings of this study indicated that FSH promoted glycolysis in epithelial ovarian cancer cells. Knockdown of PKM2 inhibited aerobic glycolysis and cell proliferation induced by FSH.

摘要

目的

细胞代谢的重编程对于肿瘤的进展是至关重要的,癌细胞中研究得最好的代谢现象是有氧糖酵解,其中丙酮酸激酶同工酶 M2(PKM2)起着关键作用。卵泡刺激素(FSH)有助于卵巢癌的进展,并且已经表明它可以调节卵巢中的细胞代谢。本研究的目的是研究 FSH 与 PKM2 之间的相互作用及其对卵巢癌细胞有氧糖酵解和增殖的影响。

方法

用不同剂量的 FSH 处理 SKOV3 和 OVCAR3 卵巢癌细胞,以研究其对细胞增殖和 PKM2 表达的影响。用 siRNA-PKM2 转染 SKOV3 和 OVCAR3 细胞,并用 FSH 处理,以检查 FSH 诱导的变化是否可以通过 siRNA-PKM2 改变。评估葡萄糖和乳酸水平,以观察这些细胞中糖酵解的变化。

结果

在本研究中,FSH 上调了 SKOV3 和 OVCAR3 细胞中 PKM2 和糖酵解的表达。PKM2 敲低减少了 FSH 诱导的细胞生长和糖酵解。此外,FSH 减弱了 PKM2 抑制诱导的细胞凋亡。

结论

总的来说,本研究的结果表明,FSH 促进了上皮性卵巢癌细胞中的糖酵解。PKM2 的敲低抑制了 FSH 诱导的有氧糖酵解和细胞增殖。

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