2. Academic Validation
  3. Targeting lectin-like oxidized low-density lipoprotein receptor-1 triggers autophagic program in esophageal cancer

Targeting lectin-like oxidized low-density lipoprotein receptor-1 triggers autophagic program in esophageal cancer

  • Cell Death Differ. 2022 Apr;29(4):697-708. doi: 10.1038/s41418-021-00884-y.
Can Li  # 1,  Fenglin Liu  # 2,  Xu Yang  # 1,  Bao Guo 1,  Guoyun Li 3,  Jie Yin 2,  Gaofei He 1,  Caiting Yang 4,  Ling Xu 1,  Shuxuan Li 1,  Hao Wu 1,  Hai Liu 4,  Yuanyuan Ruan 1,  Jianxin Gu 1,  Lan Wang 5
Affiliations

Affiliations

  • 1 NHC Key Laboratory of Glycoconjugate Research, Department of Biochemistry and Molecular Biology, School of Basic Medical Sciences, Fudan University, Shanghai, 200032, China.
  • 2 Department of General Surgery, Zhongshan Hospital, Fudan University, Shanghai, 20032, China.
  • 3 Key Laboratory of Marine Drugs of Ministry of Education, Shandong Provincial Key Laboratory of Glycoscience and Glycotechnology, School of Medicine and Pharmacy, Ocean University of China, Qingdao, 266003, China; Laboratory for Marine Drugs and Bioproducts, Pilot National Laboratory for Marine Science and Technology (Qingdao), Qingdao, 266237, China.
  • 4 Institutes of Biomedical Sciences, Shanxi University, Taiyuan, 030006, China.
  • 5 NHC Key Laboratory of Glycoconjugate Research, Department of Biochemistry and Molecular Biology, School of Basic Medical Sciences, Fudan University, Shanghai, 200032, China. wanglan@fudan.edu.cn.
  • # Contributed equally.
PMID: 34611296 DOI: 10.1038/s41418-021-00884-y
Abstract

Autophagy is a highly conserved catabolic process to maintain cellular homeostasis. However, dysfunctional Autophagy contributes to a context-dependent role in Cancer. Here, we clarified the exact role of Autophagy modulated by the scavenger receptor lectin-like oxidized low-density lipoprotein receptor-1 (LOX-1) in esophageal Cancer (EC). A comprehensive analysis in various cancers displayed that LOX-1 was upregulated the most in EC tissues and associated with poor prognosis of patients. Deletion of LOX-1 ex vivo and in vivo suppresses EC development by inducing autophagic cell death. Receptor for activated C kinase 1 (RACK1) was identified as a signal adapter of LOX-1, which incented Ras/MEK/ERK pathway and TFEB nuclear export signal and safeguarded tumorigenesis. A sulfated polysaccharide fucoidan extracted from Brown seaweed was found to bind with LOX-1 and mediate its proteasomal degradation but not the lysosome pathway, leading to autophagy-related cell death in EC. These results reveal a central contribution of LOX-1 to EC development and provide genetic ablation or bioactive polysaccharide as an effective intervention for EC therapy.

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