ArticleJournal of cellular and molecular medicine2023
A novel antimicrobial peptide M1-8 targets the lysosomal pathway to inhibit autolysosome formation and promote apoptosis in liver cancer cells.
Article in Journal of cellular and molecular medicine, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 9 citations in OpenAlex.
- Data-Driven Visualization of the Dynamics of Antimicrobial Peptides in Cell Death.Probiotics and antimicrobial proteins · 2025Review
- Myristoyl-CM4 Exhibits Direct Anticancer Activity and Immune Modulation in Hepatocellular Carcinoma: Evidence from In Vitro and Mouse Model Studies.International journal of molecular sciences · 2025Article
- Multifaceted Microneedle Patch: A One-Stop Solution to Combat Multitype Wound Infections.Biomaterials research · 2025Article
- Revisiting edible insects as sources of therapeutics and drug delivery systems for cancer therapy.Frontiers in pharmacology · 2024Review
- Application Value of Antimicrobial Peptides in Gastrointestinal Tumors.International journal of molecular sciences · 2023Review
- Recent advances and applications of peptide-agent conjugates for targeting tumor cells.Journal of cancer research and clinical oncology · 2023Review
- A novel antimicrobial peptide M1-8 targets the lysosomal pathway to inhibit autolysosome formation and promote apoptosis in liver cancer cells.Journal of cellular and molecular medicine · 2023Article
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Authors and funding
11 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Lysosomes, a central regulator of autophagy, play a critical role in tumour growth. Lysosomal protease cathepsin D can initiate apoptosis when released from lysosomes into the cytosol. In this study, we observed that Musca domestica cecropin (Mdc) 1-8 (M1-8), a small anti-tumour peptide derived from Mdc, inhibits hepatoma cell growth by blocking autophagy-lysosome fusion. This effect is likely achieved by targeting lysosomes to activate lysosomal protease D. Additionally, we examined whether lysosomal content and cathepsin D release were involved in M1-8-induced apoptosis. After exposure to M1-8, human hepatoma HepG2 cells rapidly co-localized with lysosomes, disrupted lysosomal integrity, caused leakage of lysosomal protease cathepsin D, caspase activation and mitochondrial membrane potential changes; and promoted cell apoptosis. Interestingly, in M1-8-treated HepG2 cells, autophagic protein content increased and the lysosome-autophagosome fusion was inhibited, suggesting that M1-8 can cause apoptosis through autophagy and lysosomes. This result indicates that a small accumulation of autophagy and autolysosome inhibition in cells can cause cell death. Taken together, these data suggest a novel insight into the regulatory mechanisms of M1-8 in autophagy and lysosomes, which may facilitate the development of M1-8 as a potential cancer therapeutic agent.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.