2. Academic Validation
  3. Genome-scale CRISPR screening for potential targets of ginsenoside compound K

Genome-scale CRISPR screening for potential targets of ginsenoside compound K

  • Cell Death Dis. 2020 Jan 20;11(1):39. doi: 10.1038/s41419-020-2234-5.
Yuanyuan Yang  # 1,  Xiaojian Liu  # 1,  Shuang Li 1,  Yanhao Chen 1,  Yongxu Zhao 1,  Yuda Wei 1,  Yan Qiu 1,  Yan Liu 1,  Zhihua Zhou 2,  Jun Han 3,  Guohao Wu 4,  Qiurong Ding 5 6
Affiliations

Affiliations

  • 1 CAS Key Laboratory of Nutrition, Metabolism and Food Safety, Shanghai Institute of Nutrition and Health, Shanghai Institutes for Biological Sciences, University of Chinese Academy of Sciences, Chinese Academy of Sciences, Shanghai, 200031, P. R. China.
  • 2 CAS-Key Laboratory of Synthetic Biology, Institute of Plant Physiology and Ecology, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai, 200032, China.
  • 3 Department of General Surgery, Zhongshan Hospital, Fudan University, Shanghai, China. hanjun198626@163.com.
  • 4 Department of General Surgery, Zhongshan Hospital, Fudan University, Shanghai, China. profwugh@163.com.
  • 5 CAS Key Laboratory of Nutrition, Metabolism and Food Safety, Shanghai Institute of Nutrition and Health, Shanghai Institutes for Biological Sciences, University of Chinese Academy of Sciences, Chinese Academy of Sciences, Shanghai, 200031, P. R. China. qrding@sibs.ac.cn.
  • 6 Institute for Stem Cell and Regeneration, Chinese Academy of Sciences, Beijing, 100101, P. R. China. qrding@sibs.ac.cn.
  • # Contributed equally.
PMID: 31959745 DOI: 10.1038/s41419-020-2234-5
Abstract

Ginsenosides exhibit a large variety of biological activities in maintaining physical health; however, the molecule underpinnings underlining these biological activities remain to be defined. Here, we took a cellular condition that compound K (CK) induces autophagic cell death in HeLa cells, and setup a high-throughput genetic screening using CRISPR technology. We have identified a number of CK-resistant and CK-sensitive genes, and further validated PMAIP1 as a CK-resistant gene and WASH1 as a CK-sensitive gene. Compound K treatment reduces the expression of WASH1, which further accelerates the autophagic cell death, highlighting WASH1 as an interesting downstream mediator of CK effects. Overall, our study offers an easy-to-adopt platform to study the functional mediators of ginsenosides, and provides a candidate list of genes that are potential targets of CK.

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