ArticleScientific reports2018
Chalcomoracin is a potent anticancer agent acting through triggering Oxidative stress via a mitophagy- and paraptosis-dependent mechanism.
Article in Scientific reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers, 2 of them syntheses that pooled it.
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Who cites it
33 citing papers in PubMed, 2 syntheses or guidelines pooled it, 52 citations in OpenAlex.
- Global research landscape and hotspots of paraptosis: a multi-database bibliometric analysis with a focused literature review.Frontiers in oncology · 2026Pooled it
- Guidelines for the use and interpretation of assays for monitoring autophagy (4th edition)Autophagy · 2021Guideline
- Therapeutic Potential of Mulberry and Its Resilience to Abiotic and Biotic Stresses.International journal of molecular sciences · 2026Review
- Crosstalk Between Autophagy and Paraptosis: A New Frontier in Cancer Therapy.International journal of molecular sciences · 2026Review
- Diphenyl Disulfide Induces Nonapoptotic Paraptosis in Breast Cancer Cells via ROS-Mediated ER Stress.International journal of medical sciences · 2026Article
- Paraptosis, a new type of cell death that can be applied to cancer treatment.Frontiers in oncology · 2026Review
- Copper ionophore elicits calpain-dependent paraptosis coincident with proteotoxic stress.Cell communication and signaling : CCS · 2025Article
- Review
- Organellophagy regulates cell death:A potential therapeutic target for inflammatory diseases.Journal of advanced research · 2025Review
- Mitophagy: insights into its signaling molecules, biological functions, and therapeutic potential in breast cancer.Cell death discovery · 2024Review
- Paraptosis-A Distinct Pathway to Cell Death.International journal of molecular sciences · 2024Review
- Chalcomoracin promotes apoptosis and endoplasmic reticulum stress in hepatocellular carcinoma cells.The Journal of antibiotics · 2024Article
- Targeting paraptosis in cancer: opportunities and challenges.Cancer gene therapy · 2024Review
- Sericultural By-Products: The Potential for Alternative Therapy in Cancer Drug Design.Molecules (Basel, Switzerland) · 2023Review
- Paraptosis: a unique cell death mode for targeting cancer.Frontiers in pharmacology · 2023Review
- Elicitation of Stilbenes and Benzofuran Derivatives in Hairy Root Cultures of White Mulberry (Plants (Basel, Switzerland) · 2022Article
- The emerging multifaceted role of PINK1 in cancer biology.Cancer science · 2022Review
- Isolation of Chalcomoracin as a Potential α-Glycosidase Inhibitor from Mulberry Leaves and Its Binding Mechanism.Molecules (Basel, Switzerland) · 2022Article
- Mulberry Diels-Alder-type adducts: isolation, structure, bioactivity, and synthesis.Natural products and bioprospecting · 2022Review
- Acetaldehyde Induces Cytotoxicity via Triggering Mitochondrial Dysfunction and Overactive Mitophagy.Molecular neurobiology · 2022Article
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Chalocomoracin (CMR), one of the major secondary metabolites found in fungus-infected mulberry leaves, is a potent anticancer agent. However, its anticancer mechanism remains elusive. Here, we demonstrated the potent anti-tumor activity and molecular mechanism of CMR both in vitro and in vivo. We showed for the first time that CMR treatment markedly promoted paraptosis along with extensive cytoplasmic vacuolation derived from the endoplasmic reticulum, rather than apoptosis, in PC-3 and MDA-MB-231cell lines. Additional studies revealed that ectopic expression of Myc-PINK1 (PTEN-induced kinase 1), a key regulator of mitophagy, rendered LNCap cells susceptible to CMR-induced paraptosis, suggesting that the mitophagy-dependent pathway plays a crucial role in inducing paraptosis by activating PINK1. CMR treatment directly upregulated PINK1 and downregulated Alix genes in MDA-MB-231 and PC-3 cell lines. Furthermore, mitophagy signaling and paraptosis with cytoplasmic vacuolation could be blocked by antioxidant N-acetylcysteine (NAC), indicating the novel pathway was triggered by reactive oxygen species (ROS) production. An in vivo MDA-MB-231 xenograft tumor model revealed that CMR suppressed tumor growth by inducing vacuolation production through the same signal changes as those observed in vitro. These data suggest that CMR is a potential therapeutic entity for cancer treatment through a non-apoptotic pathway.
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Registered trials
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.