代谢应激和胰腺癌的发生发展

李金涛; 雷明珠; 雷群英; 尹淼

doi:10.12182/20210160502

栏目: 综　述

代谢应激和胰腺癌的发生发展

doi: 10.12182/20210160502

李金涛^{1, 2,},
雷明珠^{1, 2},
雷群英^{1, 2, ,},
尹淼^{1, 2, ,}

1.
复旦大学附属肿瘤医院肿瘤研究所（上海 200032）
2.
复旦大学上海医学院肿瘤学系（上海 200032）

基金项目: 国家自然科学基金（No. 82002951、No. 81872240）资助

详细信息

作者简介:
雷群英，复旦大学教授，博士生导师，现任复旦大学基础医学院副院长。2014年被评为中青年科技创新领军人才，国家重点基础研究发展计划（973计划）/国家自然科学基金重大项目管理办法首席科学家。2012年获教育部自然科学奖一等奖、2013年获第十届中国青年女科学家奖、2014年获教育部自然科学奖二等奖、2019年获上海市自然科学奖一等奖。担任 Signal Transduct Target Ther 、 Cell Stress 、 Acta Biochim Biophs Sin (Shanghai) 、《中国生物化学与分子生物学报》等学术期刊编委。在 Cancer Cell、 Cell Metab、 Mol Cell、J Clin Invest 和 Nat Commun 等发表论文50余篇。主要研究方向：肿瘤代谢，Hippo-TAZ信号通路，蛋白质翻译后修饰及其生理病理效应

通讯作者:
雷群英，E-mail: qlei@fudan.edu.cn

；尹淼，E-mail：miaoyin@fudan.edu.cn

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- 被引次数: 0
出版历程
- 收稿日期: 2020-11-04
- 修回日期: 2020-12-22
- 刊出日期: 2021-01-20

A Review of Metabolic Stress and Development of Pancreatic Cancer

LI Jin-tao^{1, 2
,},
LEI Ming-zhu^{1, 2},
LEI Qun-ying^{1, 2
, ,},
YIN Miao^{1, 2
, ,}

1.
Cancer Institute, Fudan University Shanghai Cancer Center, Shanghai 200032, China
2.
Department of Oncology, Shanghai Medical College, Fudan University, Shanghai 200032, China

More Information

Corresponding author: LEI Qun-ying，E-mail: qlei@fudan.edu.cn; ；YIN Miao，E-mail：miaoyin@fudan.edu.cn

摘要

摘要: 目前胰腺导管腺癌（PDAC）的有效临床治疗方案有限，5年生存率低于8%，因此迫切需要探索新的治疗策略。PDAC为了适应极端恶劣的微环境，在其演进过程中存在广泛的代谢重编程。代谢应激与癌基因激活（如KRAS）以及抑癌基因失活所触发的信号密切相关。同时，代谢异常重塑肿瘤微环境，协同促进PDAC的发展。本篇综述将重点阐述PDAC及其微环境中的代谢重编程，以探索PDAC治疗中潜在的靶标。
- 胰腺导管腺癌 /
- 代谢 /
- 肿瘤微环境
Abstract: Pancreatic ductal adenocarcinoma (PDAC) is one of the most notorious malignancies with a 5-year survival rate of less than 8%. Therefore, it is crucial to investigate the molecular mechanism underlining PDAC initiation, promotion, and progression for efficient treatment of PDAC. In order to adapt and survive in an extremely adverse microenvironment of hypoxia and insufficiency of nutrients and energy, PDAC cells undergo extensive metabolic modification triggered by intrinsic signalings which are activated by different genetic events, including mutations occurred at KRAS, TP53, and DPC4/SMAD4, collaboratively promoting PDAC development. Notably, PDCA cells have extensive crosstalk in the form of reciprocal metabolic flux with its surrounding microenvironment to facilitate tumor advancement and therapy resistance. We herein summarize recent findings of PDAC metabolism and discuss metabolic rewiring-based therapeutic strategies.
- Pancreatic ductal adenocarcinoma /
- Metabolism /
- Tumor microenvironment

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参考文献(60)

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