Nature Communications (Jun 2019)
Identification of metabolic vulnerabilities of receptor tyrosine kinases-driven cancer
- Nan Jin,
- Aiwei Bi,
- Xiaojing Lan,
- Jun Xu,
- Xiaomin Wang,
- Yingluo Liu,
- Ting Wang,
- Shuai Tang,
- Hanlin Zeng,
- Ziqi Chen,
- Minjia Tan,
- Jing Ai,
- Hua Xie,
- Tao Zhang,
- Dandan Liu,
- Ruimin Huang,
- Yue Song,
- Elaine Lai-Han Leung,
- Xiaojun Yao,
- Jian Ding,
- Meiyu Geng,
- Shu-Hai Lin,
- Min Huang
Affiliations
- Nan Jin
- Division of Antitumor Pharmacology, State Key Laboratory of Drug Research, Shanghai Institute of Materia Medica, Chinese Academy of Sciences
- Aiwei Bi
- Division of Antitumor Pharmacology, State Key Laboratory of Drug Research, Shanghai Institute of Materia Medica, Chinese Academy of Sciences
- Xiaojing Lan
- Division of Antitumor Pharmacology, State Key Laboratory of Drug Research, Shanghai Institute of Materia Medica, Chinese Academy of Sciences
- Jun Xu
- Division of Antitumor Pharmacology, State Key Laboratory of Drug Research, Shanghai Institute of Materia Medica, Chinese Academy of Sciences
- Xiaomin Wang
- Division of Antitumor Pharmacology, State Key Laboratory of Drug Research, Shanghai Institute of Materia Medica, Chinese Academy of Sciences
- Yingluo Liu
- Division of Antitumor Pharmacology, State Key Laboratory of Drug Research, Shanghai Institute of Materia Medica, Chinese Academy of Sciences
- Ting Wang
- Division of Antitumor Pharmacology, State Key Laboratory of Drug Research, Shanghai Institute of Materia Medica, Chinese Academy of Sciences
- Shuai Tang
- Division of Antitumor Pharmacology, State Key Laboratory of Drug Research, Shanghai Institute of Materia Medica, Chinese Academy of Sciences
- Hanlin Zeng
- Division of Antitumor Pharmacology, State Key Laboratory of Drug Research, Shanghai Institute of Materia Medica, Chinese Academy of Sciences
- Ziqi Chen
- Division of Antitumor Pharmacology, State Key Laboratory of Drug Research, Shanghai Institute of Materia Medica, Chinese Academy of Sciences
- Minjia Tan
- University of Chinese Academy of Sciences
- Jing Ai
- Division of Antitumor Pharmacology, State Key Laboratory of Drug Research, Shanghai Institute of Materia Medica, Chinese Academy of Sciences
- Hua Xie
- Division of Antitumor Pharmacology, State Key Laboratory of Drug Research, Shanghai Institute of Materia Medica, Chinese Academy of Sciences
- Tao Zhang
- Division of Antitumor Pharmacology, State Key Laboratory of Drug Research, Shanghai Institute of Materia Medica, Chinese Academy of Sciences
- Dandan Liu
- University of Chinese Academy of Sciences
- Ruimin Huang
- University of Chinese Academy of Sciences
- Yue Song
- Agilent Technologies (China) Co., Ltd.
- Elaine Lai-Han Leung
- Macau Institute for Applied Research in Medicine and Health, State Key Laboratory of Quality Research in Chinese Medicine, Macau University of Science and Technology
- Xiaojun Yao
- Macau Institute for Applied Research in Medicine and Health, State Key Laboratory of Quality Research in Chinese Medicine, Macau University of Science and Technology
- Jian Ding
- Division of Antitumor Pharmacology, State Key Laboratory of Drug Research, Shanghai Institute of Materia Medica, Chinese Academy of Sciences
- Meiyu Geng
- Division of Antitumor Pharmacology, State Key Laboratory of Drug Research, Shanghai Institute of Materia Medica, Chinese Academy of Sciences
- Shu-Hai Lin
- State Key Laboratory of Cellular Stress Biology, Innovation Center for Cell Signaling Network, School of Life Sciences, Xiamen University
- Min Huang
- Division of Antitumor Pharmacology, State Key Laboratory of Drug Research, Shanghai Institute of Materia Medica, Chinese Academy of Sciences
- DOI
- https://doi.org/10.1038/s41467-019-10427-2
- Journal volume & issue
-
Vol. 10,
no. 1
pp. 1 – 15
Abstract
Cancer subtypes may have distinct metabolic vulnerabilities that can be exploited for therapeutic interventions. Here, the authors show that in lung cancer, genetic activation of distinct oncogenic receptor tyrosine kinases results in unique metabolic liabilities and, in particular, EGFR aberrant cancers rely on the serine biosynthetic pathway while FGFR aberrant cancers rely on glycolysis.
