The interactive role of inflammatory mediators and metabolic reprogramming in pancreatic cancer.

The interactive role of inflammatory mediators and metabolic reprogramming in pancreatic cancer.
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DOI:
10.1016/j.trecan.2022.03.004
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发表时间:
2022-07
期刊:
影响因子:
18.4
通讯作者:
Hussain SP
Hussain SP
中科院分区:
医学1区
文献类型:
--
作者:
Ohara Y;Valenzuela P;Hussain SP

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胰腺导管腺癌(PDAC)的特点是其高度反应性炎症促纤维增生性基质,有证据表明广泛的肿瘤基质相互作用主要由炎症因子介导。 KRAS 突变和炎症信号传导可促进促肿瘤发生事件,包括代谢重编程与多种调节间串扰,以满足能量的高需求并调节肿瘤生长和进展的氧化应激。值得注意的是,PDAC 更具攻击性的分子亚型可增强糖酵解中间体的流入。本综述重点关注炎症信号传导和代谢重编程的相互作用,以及新出现的串扰证据,支持 PDAC 的发生、进展和治疗耐药。了解炎症和代谢适应之间新出现的串扰可能会确定潜在的靶点并开发新的 PDAC 治疗方法。
Pancreatic ductal adenocarcinoma (PDAC) is characterized by its highly reactive inflammatory desmoplastic stroma with evidence of an extensive tumor stromal interaction largely mediated by inflammatory factors. KRAS mutation and inflammatory signaling promote pro-tumorigenic events including metabolic reprogramming with several inter-regulatory crosstalk to fulfill the high demand of energy and regulate oxidative stress for tumor growth and progression. Notably, the more aggressive molecular subtype of PDAC enhances influx of glycolytic intermediates. This review focuses on the interactive role of inflammatory signaling and metabolic reprogramming with emerging evidence of crosstalk, which supports the development, progression, and therapeutic resistance of PDAC. Understanding the emerging crosstalk between inflammation and metabolic adaptations may identify potential targets and develop novel therapeutic approaches for PDAC.
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