Oncogenic KRAS triggers metabolic reprogramming in pancreatic ductal adenocarcinoma

被引：7
|
作者：
Shen, Xuqing [1 ]
Niu, Ningning [1 ]
Xue, Jing [1 ]
机构：
[1] Shanghai Jiao Tong Univ, State Key Lab Oncogenes & Related Genes, Stem Cell Res Ctr, Ren Ji Hosp,Sch Med,Shanghai Canc Inst, Shanghai 200127, Peoples R China
来源：
JOURNAL OF TRANSLATIONAL INTERNAL MEDICINE | 2023年 / 11卷 / 04期
基金：
中国国家自然科学基金;
关键词：
pancreatic ductal adenocarcinoma; oncogenic KRAS activation; metabolic reprogramming; POSITRON-EMISSION-TOMOGRAPHY; FATTY-ACID-METABOLISM; GLUTAMINE-METABOLISM; TUMOR-GROWTH; GEMCITABINE RESISTANCE; CANCER GROWTH; CELL-GROWTH; K-RAS; GLUCOSE; INHIBITOR;
D O I：
10.2478/jtim-2022-0022
中图分类号：
R5 [内科学];
学科分类号：
1002 ; 100201 ;
摘要：
Pancreatic ductal adenocarcinoma (PDAC) is a devastating disease with an extremely high lethality rate. Oncogenic KRAS activation has been proven to be a key driver of PDAC initiation and progression. There is increasing evidence that PDAC cells undergo extensive metabolic reprogramming to adapt to their extreme energy and biomass demands. Cell-intrinsic factors, such as KRAS mutations, are able to trigger metabolic rewriting. Here, we update recent advances in KRAS-driven metabolic reprogramming and the associated metabolic therapeutic potential in PDAC.
引用
收藏
页码：322 / 329
页数：8
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