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

页码：322 / 329

页数：8

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