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ID 116604
Han, Zhu Sichuan University
Zhang, Weizhi Huazhong University of Science and Technology
Ning, Wanshan Huazhong University of Science and Technology
Wang, Chenwei Huazhong University of Science and Technology
Deng, Wankun Huazhong University of Science and Technology
Li, Zhidan Sichuan University
Shang, Zehua Sichuan University
Shen, Xiaofei Chengdu University
Liu, Xiaohui Tsinghua University
Chen, Lu Sichuan University
Xue, Yu Huazhong University of Science and Technology|Nanjing University
Jia, Da Sichuan University
Content Type
Journal Article
Autophagy can selectively target protein aggregates, pathogens, and dysfunctional organelles for the lysosomal degradation. Aberrant regulation of autophagy promotes tumorigenesis, while it is far less clear whether and how tumor-specific alterations result in autophagic aberrance. To form a link between aberrant autophagy selectivity and human cancer, we establish a computational pipeline and prioritize 222 potential LIR (LC3-interacting region) motif-associated mutations (LAMs) in 148 proteins. We validate LAMs in multiple proteins including ATG4B, STBD1, EHMT2 and BRAF that impair their interactions with LC3 and autophagy activities. Using a combination of transcriptomic, metabolomic and additional experimental assays, we show that STBD1, a poorly-characterized protein, inhibits tumor growth via modulating glycogen autophagy, while a patient-derived W203C mutation on LIR abolishes its cancer inhibitory function. This work suggests that altered autophagy selectivity is a frequently-used mechanism by cancer cells to survive during various stresses, and provides a framework to discover additional autophagy-related pathways that influence carcinogenesis.
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Nature Communications
Springer Nature
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Oral Sciences