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hENT1 Reverses Chemoresistance by Regulating Glycolysis in Pancreatic Cancer
Cancer Letters ( IF 9.7 ) Pub Date : 2020-03-18 , DOI: 10.1016/j.canlet.2020.03.015
Yun Xi , Peng Yuan , Ting Li , Min Zhang , Mo-Fang Liu , Biao Li

Gemcitabine (GEM) chemotherapy, as the first-line regimen for pancreatic cancer, tends to induce drug resistance, which ultimately worsens the prognosis of patients with pancreatic cancer. Our previous study indicated a close correlation between pancreatic cancer progression and glucose metabolism, especially at the chemoresistant stage, highlighting the importance of the application of 18F-FDG PET dual-phase imaging in the early detection of pancreatic cancer. We speculate that glycolysis, participates in the development of chemoresistance in pancreatic cancer. In this article, we wanted to determine whether manipulating hENT1 expression in pancreatic cancer cells can reverse GEM chemoresistance and whether glucose transport and glycolysis are involved during this process. We found that hENT1 reversed GEM-induced drug resistance by inhibiting glycolysis and altering glucose transport mediated by HIF-1α in pancreatic cancer. Our findings also suggest that 18F-FDG PET dual-phase imaging after the 4th chemotherapy treatment can accurately identify drug-resistant pancreatic tumors and improve hENT1 reversal therapy. Our findings highlight that the dynamic observation of (retention index) RI changes from the beginning of treatment can also be helpful for evaluating the therapeutic effect.



中文翻译:

hENT1通过调节胰腺癌糖酵解逆转化学耐药性

吉西他滨(GEM)化疗作为胰腺癌的一线治疗方案,易于诱导耐药性,最终使胰腺癌患者的预后恶化。我们先前的研究表明,胰腺癌进展与葡萄糖代谢密切相关,特别是在化学抗药性阶段,强调了应用18F-FDG PET双相成像可早期检测胰腺癌。我们推测糖酵解参与胰腺癌的化学抗性发展。在本文中,我们想确定在胰腺癌细胞中操纵hENT1表达是否可以逆转GEM化学耐药性以及在此过程中是否涉及葡萄糖转运和糖酵解。我们发现hENT1通过抑制糖酵解和改变胰腺癌中HIF-1α介导的葡萄糖转运来逆转GEM诱导的耐药性。我们的发现还表明,第四成像后18 F-FDG PET双相成像化学疗法可以准确地识别耐药的胰腺肿瘤并改善hENT1逆转疗法。我们的发现表明,从治疗开始就动态观察(保留指数)RI变化也有助于评估治疗效果。

更新日期:2020-03-19
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