CC-223、NSC781406和BGT226通过mTOR信号通路对胰腺癌细胞发挥细胞毒性作用。
CC-223, NSC781406, and BGT226 Exerts a Cytotoxic Effect Against Pancreatic Cancer Cells via mTOR Signaling.
作者信息
Guo Yangyang, Zhu Hengyue, Weng Min, Zhang Hewei, Wang Cheng, Sun Linxiao
机构信息
Key Laboratory of Diagnosis and Treatment of Severe Hepato-Pancreatic Diseases of Zhejiang Province, Zhejiang Provincial Top Key Discipline in Surgery, Wenzhou Medical University First Affiliated Hospital, Wenzhou, China.
出版信息
Front Pharmacol. 2020 Nov 11;11:580407. doi: 10.3389/fphar.2020.580407. eCollection 2020.
The mTOR signaling pathway is abnormally activated in pancreatic cancer and is related to tumor glucose metabolism. However, its specific regulation mechanism is still unclear. Therefore, this study aims to investigate whether Sestrin2 affects the glucose metabolism of pancreatic cancer by modulating mTOR signal and then affects its biological behavior. We have observed that l-leucine can promote the proliferation of pancreatic cancer cells and increase the expression of Sestrin2 and p-mTOR proteins. In order to further study the role of Sestrin2 and mTOR signaling in pancreatic cancer, we conducted Sestrin2 overexpression and mTOR pharmacological inhibition experiments. We found that Sestrin2 overexpression can increase glycolysis of pancreatic cancer cells and promote their proliferation. This effect can be eliminated by mTOR inhibitors. Finally, we found that Sestrin2 knockdown could inhibit the growth of pancreatic cancer . In conclusion, these findings suggest that Sestrin2 may promote the occurrence and development of pancreatic cancer through mTOR signaling.
mTOR信号通路在胰腺癌中异常激活，且与肿瘤葡萄糖代谢相关。然而，其具体调控机制仍不清楚。因此，本研究旨在探究Sestrin2是否通过调节mTOR信号影响胰腺癌的葡萄糖代谢，进而影响其生物学行为。我们观察到L-亮氨酸可促进胰腺癌细胞增殖，并增加Sestrin2和p-mTOR蛋白的表达。为进一步研究Sestrin2和mTOR信号在胰腺癌中的作用，我们进行了Sestrin2过表达和mTOR药理学抑制实验。我们发现Sestrin2过表达可增加胰腺癌细胞的糖酵解并促进其增殖。这种作用可被mTOR抑制剂消除。最后，我们发现敲低Sestrin2可抑制胰腺癌生长。总之，这些发现表明Sestrin2可能通过mTOR信号促进胰腺癌的发生发展。
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