Nature Communications (Jul 2022)
The cholesterol uptake regulator PCSK9 promotes and is a therapeutic target in APC/KRAS-mutant colorectal cancer
- Chi Chun Wong,
- Jian-Lin Wu,
- Fenfen Ji,
- Wei Kang,
- Xiqing Bian,
- Huarong Chen,
- Lam-Shing Chan,
- Simson Tsz Yat Luk,
- Samuel Tong,
- Jiaying Xu,
- Qiming Zhou,
- Dabin Liu,
- Hao Su,
- Hongyan Gou,
- Alvin Ho-Kwan Cheung,
- Ka Fai To,
- Zongwei Cai,
- Jerry W. Shay,
- Jun Yu
Affiliations
- Chi Chun Wong
- Institute of Digestive Disease, Department of Medicine and Therapeutics, State Key Laboratory of Digestive Disease, Li Ka Shing Institute of Health Sciences, The Chinese University of Hong Kong
- Jian-Lin Wu
- State Key Laboratory of Quality Research in Chinese Medicine, Macau Institute for Applied Research in Medicine and Health, Macau University of Science and Technology
- Fenfen Ji
- Institute of Digestive Disease, Department of Medicine and Therapeutics, State Key Laboratory of Digestive Disease, Li Ka Shing Institute of Health Sciences, The Chinese University of Hong Kong
- Wei Kang
- Department of Anatomical and Cellular Pathology, The Chinese University of Hong Kong
- Xiqing Bian
- State Key Laboratory of Quality Research in Chinese Medicine, Macau Institute for Applied Research in Medicine and Health, Macau University of Science and Technology
- Huarong Chen
- Institute of Digestive Disease, Department of Medicine and Therapeutics, State Key Laboratory of Digestive Disease, Li Ka Shing Institute of Health Sciences, The Chinese University of Hong Kong
- Lam-Shing Chan
- Institute of Digestive Disease, Department of Medicine and Therapeutics, State Key Laboratory of Digestive Disease, Li Ka Shing Institute of Health Sciences, The Chinese University of Hong Kong
- Simson Tsz Yat Luk
- Institute of Digestive Disease, Department of Medicine and Therapeutics, State Key Laboratory of Digestive Disease, Li Ka Shing Institute of Health Sciences, The Chinese University of Hong Kong
- Samuel Tong
- Institute of Digestive Disease, Department of Medicine and Therapeutics, State Key Laboratory of Digestive Disease, Li Ka Shing Institute of Health Sciences, The Chinese University of Hong Kong
- Jiaying Xu
- Institute of Digestive Disease, Department of Medicine and Therapeutics, State Key Laboratory of Digestive Disease, Li Ka Shing Institute of Health Sciences, The Chinese University of Hong Kong
- Qiming Zhou
- Institute of Digestive Disease, Department of Medicine and Therapeutics, State Key Laboratory of Digestive Disease, Li Ka Shing Institute of Health Sciences, The Chinese University of Hong Kong
- Dabin Liu
- Institute of Digestive Disease, Department of Medicine and Therapeutics, State Key Laboratory of Digestive Disease, Li Ka Shing Institute of Health Sciences, The Chinese University of Hong Kong
- Hao Su
- Institute of Digestive Disease, Department of Medicine and Therapeutics, State Key Laboratory of Digestive Disease, Li Ka Shing Institute of Health Sciences, The Chinese University of Hong Kong
- Hongyan Gou
- Institute of Digestive Disease, Department of Medicine and Therapeutics, State Key Laboratory of Digestive Disease, Li Ka Shing Institute of Health Sciences, The Chinese University of Hong Kong
- Alvin Ho-Kwan Cheung
- Department of Anatomical and Cellular Pathology, The Chinese University of Hong Kong
- Ka Fai To
- Department of Anatomical and Cellular Pathology, The Chinese University of Hong Kong
- Zongwei Cai
- State Key Laboratory of Environmental and Biological Analysis, Department of Chemistry, Hong Kong Baptist University
- Jerry W. Shay
- Department of Cell Biology, University of Texas Southwestern Medical Center
- Jun Yu
- Institute of Digestive Disease, Department of Medicine and Therapeutics, State Key Laboratory of Digestive Disease, Li Ka Shing Institute of Health Sciences, The Chinese University of Hong Kong
- DOI
- https://doi.org/10.1038/s41467-022-31663-z
- Journal volume & issue
-
Vol. 13,
no. 1
pp. 1 – 15
Abstract
Looking for metabolic-associated vulnerabilities is a promising approach for therapeutic intervention in KRAS-mutant colorectal cancer. Here, the authors show that the cholesterol-uptake regulator PCSK9 drives tumourigenesis and is a therapeutic target in KRASmutant colorectal cancer.
