ArticleCell biology and toxicology2017
Disruption of endolysosomal trafficking pathways in glioma cells by methuosis-inducing indole-based chalcones.
Article in Cell biology and toxicology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers, 1 of them a synthesis that pooled it.
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Who cites it
18 citing papers in PubMed, 1 synthesis or guideline pooled it, 42 citations in OpenAlex.
- Metabolic cell death in cancer: mechanisms and therapeutic potential.Apoptosis : an international journal on programmed cell death · 2025Pooled it
- Cytoskeleton disruption and plasma membrane damage determine methuosis of normal and malignant cells.Cell & bioscience · 2025Article
- Exosome: an overview on enhanced biogenesis by small molecules.Naunyn-Schmiedeberg's archives of pharmacology · 2025Review
- Repurposing methuosis-inducing anticancer drugs for anthelmintic therapy.PLoS pathogens · 2024Review
- Forms of Non-Apoptotic Cell Death and Their Role in Gliomas-Presentation of the Current State of Knowledge.Biomedicines · 2024Review
- Studies on Autophagy and Apoptosis of Fibrosarcoma HT-1080 Cells Mediated by Chalcone with Indole Moiety.International journal of molecular sciences · 2024Article
- Perinuclear damage from nuclear envelope deterioration elicits stress responses that contribute toScience advances · 2024Article
- Methuosis Contributes to Jaspine-B-Induced Cell Death.International journal of molecular sciences · 2022Article
- Investigating Nonapoptotic Cell Death Using Chemical Biology Approaches.Cell chemical biology · 2020Review
- Ethanol Extract of the Infructescence ofEvidence-based complementary and alternative medicine : eCAM · 2020Article
- The Dual Role of Macropinocytosis in Cancers: Promoting Growth and Inducing Methuosis to Participate in Anticancer Therapies as Targets.Frontiers in oncology · 2020Review
- Combined mTORC1/mTORC2 inhibition blocks growth and induces catastrophic macropinocytosis in cancer cells.Proceedings of the National Academy of Sciences of the United States of America · 2019Article
- Cathepsin B: A sellsword of cancer progression.Cancer letters · 2019Review
- The JNK signaling pathway plays a key role in methuosis (non-apoptotic cell death) induced by MOMIPP in glioblastoma.BMC cancer · 2019Article
- Vacuole-inducing compounds that disrupt endolysosomal trafficking stimulate production of exosomes by glioblastoma cells.Molecular and cellular biochemistry · 2018Article
- Assessments of iodoindoles and abamectin as inducers of methuosis in pinewood nematode, Bursaphelenchus xylophilus.Scientific reports · 2017Article
- [Mechanism of Platycarya strobilacea Sieb. et Zucc extract-induced methuosis in human nasopharyngeal carcinoma CNE1 and CNE2 cells].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2017Article
- Glioblastoma cytotoxicity conferred through dual disruption of endolysosomal homeostasis by Vacquinol-1.Neuro-oncology advancesArticle
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Methuosis is a form of non-apoptotic cell death involving massive vacuolization of macropinosome-derived endocytic compartments, followed by a decline in metabolic activity and loss of membrane integrity. To explore the induction of methuosis as a potential therapeutic strategy for killing cancer cells, we have developed small molecules (indole-based chalcones) that trigger this form of cell death in glioblastoma and other cancer cell lines. Here, we report that in addition to causing fusion and expansion of macropinosome compartments, the lead compound, 3-(5-methoxy-2-methyl-1H-indol-3-yl)-1-(4-pyridinyl)-2-propen-1-one (MOMIPP), disrupts vesicular trafficking at the lysosomal nexus, manifested by impaired degradation of EGF and LDL receptors, defective processing of procathepsins, and accumulation of autophagosomes. In contrast, secretion of the ectodomain derived from a prototypical type-I membrane glycoprotein, β-amyloid precursor protein, is increased rather than diminished. A closely related MOMIPP analog, which causes substantial vacuolization without reducing cell viability, also impedes cathepsin processing and autophagic flux, but has more modest effects on receptor degradation. A third analog, which causes neither vacuolization nor loss of viability, has no effect on endolysosomal trafficking. The results suggest that differential cytotoxicity of structurally similar indole-based chalcones is related, at least in part, to the severity of their effects on endolysosomal trafficking pathways.
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