ArticleOncogene2020
A cell-penetrating MARCKS mimetic selectively triggers cytolytic death in glioblastoma.
Article in Oncogene, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
12 citing papers in PubMed, 20 citations in OpenAlex.
- MARCKS as a mediator and target for pathological tunneling nanotubes between patient-derived glioblastoma cells and astrocytes.Cell death & disease · 2026Article
- No differences in therapeutic efficacy while sparing healthy tissue for orthotopic glioblastoma patient-derived xenografts in context of proton FLASH.Clinical and translational radiation oncology · 2026Article
- Xenoline-polarized macrophages as an alternative in vitro model of tumor-associated macrophages in glioblastoma.Acta neuropathologica communications · 2025Article
- Altering fractionation during radiation overcomes radio-resistance in patient-derived glioblastoma cells assessed using a novel longitudinal radiation cytotoxicity assay.Radiotherapy and oncology : journal of the European Society for Therapeutic Radiology and Oncology · 2025Article
- MARCKS Inhibition Alters Bovine Neutrophil Responses toBiomedicines · 2024Article
- Antitumor effects of chemically modified miR-143 lipoplexes in a mouse model of pelvic colorectal cancer via myristoylated alanine-rich C kinase substrate downregulation.Molecular therapy. Nucleic acids · 2023Article
- Small Organic Compounds Mimicking the Effector Domain of Myristoylated Alanine-Rich C-Kinase Substrate Stimulate Female-Specific Neurite Outgrowth.International journal of molecular sciences · 2023Article
- Review
- An in vivo model of glioblastoma radiation resistance identifies long noncoding RNAs and targetable kinases.JCI insight · 2022Article
- Combination of cell-penetrating peptides with nanomaterials for the potential therapeutics of central nervous system disorders: a review.Journal of nanobiotechnology · 2021Review
- Challenges and Opportunities of Targeting Astrocytes to Halt Neurodegenerative Disorders.Cells · 2021Review
- N-cadherin upregulation mediates adaptive radioresistance in glioblastoma.The Journal of clinical investigation · 2021Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
12 authors at 1 institution in 1 country.
Funding
Abstract
Glioblastoma (GBM) is an aggressive malignancy with limited effectiveness of standard of care therapies including surgery, radiation, and temozolomide chemotherapy necessitating novel therapeutics. Unfortunately, GBMs also harbor several signaling alterations that protect them from traditional therapies that rely on apoptotic programmed cell death. Because almost all GBM tumors have dysregulated phosphoinositide signaling as part of that process, we hypothesized that peptide mimetics derived from the phospholipid binding domain of Myristoylated alanine-rich C-kinase substrate (MARCKS) could serve as a novel GBM therapeutic. Using molecularly classified patient-derived xenograft (PDX) lines, cultured in stem-cell conditions, we demonstrate that cell permeable MARCKS effector domain (ED) peptides potently target all GBM molecular classes while sparing normal human astrocytes. Cell death mechanistic testing revealed that these peptides produce rapid cytotoxicity in GBM that overcomes caspase inhibition. Moreover, we identify a GBM-selective cytolytic death mechanism involving plasma membrane targeting and intracellular calcium accumulation. Despite limited relative partitioning to the brain, tail-vein peptide injection revealed tumor targeting in intracranially implanted GBM PDX. These results indicate that MARCKS ED peptide therapeutics may overcome traditional GBM resistance mechanisms, supporting further development of similar agents.
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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.