Key Laboratory of Marine Drugs, Chinese Ministry of Education, School of Medicine and Pharmacy, Ocean University of China, Qingdao, 266003, PR China.
Key Laboratory of Marine Drugs, Chinese Ministry of Education, School of Medicine and Pharmacy, Ocean University of China, Qingdao, 266003, PR China; Laboratory for Marine Drugs and Bioproducts of Qingdao National Laboratory for Marine Science and Technology, Qingdao, 266237, PR China; Open Studio for Druggability Research of Marine Natural Products, Pilot National Laboratory for Marine Science and Technology (Qingdao), Qingdao, 266237, PR China.
Biochem Biophys Res Commun. 2020 Jul 30;528(3):594-600. doi: 10.1016/j.bbrc.2020.05.139. Epub 2020 Jun 5.
Pyruvate kinase M2 (PKM2) functions as an important rate-limiting enzyme of aerobic glycolysis that is involved in tumor initiation and progression. However, there are few studies on effective PKM2 inhibitors. Gliotoxin is a marine-derived fungal secondary metabolite with multiple biological activities, including immunosuppression, cytotoxicity, and et al. In this study, we found that Gliotoxin directly bound to PKM2 and inhibited its glycolytic activity in a dose-dependent manner accompanied by the decreases in glucose consumption and lactate production in the human glioma cell line U87. Moreover, Gliotoxin suppressed tyrosine kinase activity of PKM2, leading to a dramatic reduction in Stat3 phosphorylation in U87 cells. Furthermore, Gliotoxin suppressed cell viability in U87 cells, and cytotoxicity of Gliotoxin on U87 cells was obviously augmented under hypoxia condition compared to normal condition. Finally, Gliotoxin was demonstrated to induce cell apoptosis of U87 cells and synergize with temozolomide. Our findings identify Gliotoxin as a new PKM2 inhibitor with anti-tumor activity, which lays the foundation for the development of Gliotoxin as a promising anti-tumor drug in the future.
丙酮酸激酶 M2(PKM2)作为有氧糖酵解的重要限速酶,参与肿瘤的发生和发展。然而,目前针对有效的 PKM2 抑制剂的研究较少。吉罗毒素是一种海洋来源的真菌次级代谢产物,具有多种生物学活性,包括免疫抑制、细胞毒性等。在本研究中,我们发现吉罗毒素可直接与 PKM2 结合,并呈剂量依赖性抑制其糖酵解活性,伴随人神经胶质瘤细胞系 U87 中葡萄糖消耗和乳酸生成减少。此外,吉罗毒素抑制 PKM2 的酪氨酸激酶活性,导致 U87 细胞中 Stat3 磷酸化显著减少。进一步研究发现,吉罗毒素抑制 U87 细胞活力,且在缺氧条件下,吉罗毒素对 U87 细胞的细胞毒性明显高于正常条件。最后,吉罗毒素诱导 U87 细胞凋亡,并与替莫唑胺协同作用。本研究鉴定了吉罗毒素作为一种具有抗肿瘤活性的新型 PKM2 抑制剂,为未来将吉罗毒素开发为一种有前途的抗肿瘤药物奠定了基础。