熊果酸通过KLF5/PI3K/AKT信号通路抑制卵巢癌糖酵解

The American journal of Chinese medicine Pub Date : 2024-01-01 Epub Date: 2024-11-29 DOI:10.1142/S0192415X2450085X
Meng Xu, Xiaoqi Li, Chenyue Yuan, Tingting Zhu, Mengfei Wang, Ying Zhu, Yanqiu Duan, Jialiang Yao, Bin Luo, Ziliang Wang, Sheng Yin, Yuqing Zhao
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引用次数: 0

摘要

糖酵解是卵巢癌的关键代谢重编程特征之一。熊果酸(UA)作为一种天然化合物,对肿瘤代谢具有有益的调节作用。在本研究中,我们通过RNA-seq分析和一系列体外和体内功能实验证实,UA显著抑制卵巢癌细胞增殖,促进肿瘤凋亡,降低糖酵解水平。此外,在体外和体内实验中,它显示出与顺铂的协同治疗作用。此外,在分子水平上,我们发现UA通过与转录因子KLF5结合,阻断下游PI3K/AKT信号通路的转录表达,从而抑制卵巢癌的糖酵解,从而发挥其治疗作用。综上所述,我们的研究表明,UA可以通过KLF5/PI3K/AKT信号轴抑制卵巢癌细胞的增殖、凋亡和糖酵解水平。我们的研究结果为天然化合物UA在卵巢癌中的治疗应用提供了新的视角,并支持其作为化疗候选药物的潜在发展。
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Ursolic Acid Inhibits Glycolysis of Ovarian Cancer via KLF5/PI3K/AKT Signaling Pathway.

Glycolysis is one of the key metabolic reprogramming characteristics of ovarian cancer. Ursolic Acid (UA), as a natural compound, exerts a beneficial regulatory effect on tumor metabolism. In this study, we have confirmed through RNA-seq analysis and a series of in vitro and in vivo functional experiments that UA significantly inhibits ovarian cancer cell proliferation, promotes tumor apoptosis, and reduces glycolysis levels. Additionally, it demonstrates synergistic therapeutic effects with cisplatin in both in vitro and in vivo experiments. Furthermore, at the molecular level, we found that UA inhibits glycolysis in ovarian cancer by binding to the transcription factor KLF5 and blocking the transcriptional expression of the downstream PI3K/AKT signaling pathway, thereby exerting its therapeutic effect. In conclusion, our research indicates that UA can inhibit the proliferation, apoptosis, and glycolysis levels of ovarian cancer cells through the KLF5/PI3K/AKT signaling axis. Our findings offer a new perspective on the therapeutic application of the natural compound UA in ovarian cancer and support its potential development as a candidate for chemotherapy.

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