Limin Feng
Current Organizations / Institutes
The organizations/institutes from the scholar's latest article
Research Subjects
Research Interests
Limin Feng has a total of 4 co-authors. Here are the top co-authors by number of shared publications:
- Chung-Kuang Lu
National Research Institute of Chinese Medicine, Ministry of Health and Welfare, Taipei 11221, Taiwan
1 shared publication - Jiajun Wu
State Key Laboratory of Marine Pollution and Department of Biomedical Sciences, University of Hong Kong, Hong Kong SAR 999077, China
1 shared publication - Jianbo Yue
Division of Natural and Applied Sciences, Synear Molecular Biology Lab, Duke Kunshan University, China
1 shared publication - Leo Lai Chan
State Key Laboratory of Marine Environmental Health, City University of Hong Kong, Kowloon Tong, Hong Kong, China
1 shared publication
Latest Publications
- Open Access
- 10 January 2023
- Published by MDPI AG in Marine Drugs
- Vol. 21 (1) , 46
Identification of Anhydrodebromoaplysiatoxin as a Dichotomic Autophagy Inhibitor
Dysfunctional autophagy is associated with various human diseases, e.g., cancer. The discovery of small molecules modulating autophagy with therapeutic potential could be significant. To this end, we screened the ability of a series of metabolites isolated from marine microorganisms to modulate autophagy. Anhydrodebromoaplysiatoxin (ADAT), a metabolite yielded by the marine red algae Gracilaria coronopifolia, inhibited autophagosome-lysosome fusion in mammalian cells, thereby inducing the accumulation of autophagosomes. Treatment of cells with ADAT alkalinized lysosomal pH. Interestingly, ADAT also activated the mTOR/p70S6K/FoxO3a signaling pathway, likely leading to the inhibition of autophagy induction. ADAT had little effect on apoptosis. Our results suggest that ADAT is a dichotomic autophagy inhibitor that inhibits both late-stage (autophagosome-lysosome fusion) and early-stage (autophagy induction) autophagy.
- 10 January 2023
- Published by MDPI AG in Marine Drugs
- Vol. 21 (1) , 46
Open AccessIdentification of Anhydrodebromoaplysiatoxin as a Dichotomic Autophagy Inhibitor
Dysfunctional autophagy is associated with various human diseases, e.g., cancer. The discovery of small molecules modulating autophagy with therapeutic potential could be significant. To this end, we screened the ability of a series of metabolites isolated from marine microorganisms to modulate autophagy. Anhydrodebromoaplysiatoxin (ADAT), a metabolite yielded by the marine red algae Gracilaria coronopifolia, inhibited autophagosome-lysosome fusion in mammalian cells, thereby inducing the accumulation of autophagosomes. Treatment of cells with ADAT alkalinized lysosomal pH. Interestingly, ADAT also activated the mTOR/p70S6K/FoxO3a signaling pathway, likely leading to the inhibition of autophagy induction. ADAT had little effect on apoptosis. Our results suggest that ADAT is a dichotomic autophagy inhibitor that inhibits both late-stage (autophagosome-lysosome fusion) and early-stage (autophagy induction) autophagy.