ArticleCell death discovery2023
PME-1 sensitizes glioblastoma cells to oxidative stress-induced cell death by attenuating PP2A-B55α-mediated inactivation of MAPKAPK2-RIPK1 signaling.
Article in Cell death discovery, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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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.
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Who cites it
5 citing papers in PubMed, 7 citations in OpenAlex.
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- Phosphatases in tumor cell immune escape: a perspective based on the camouflage, coercion, cytoprotection.Frontiers in cell and developmental biology · 2026Review
- Review
- A Small Molecule Inhibitor of Leucine Carboxyl Methyltransferase-1 Inhibits Cancer Cell Survival.Frontiers in drug discovery · 2024Article
- Article
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
Glioblastoma (GBM) is the most common primary brain tumor in adults. Current standard therapy is surgery followed by radiotherapy, with concurrent and adjuvant temozolomide chemotherapy. GBM is characterized by almost uniformly fatal outcomes, highlighting the unmet clinical need for more efficient, biomarker-guided treatments. Protein phosphatase methylesterase-1 (PME-1), a regulator of the tumor suppressive phosphatase PP2A, promotes PP2A demethylation and inactivation, and is overexpressed in 44% of GBM, associated with increased tumor grade and cellular proliferation. Here, we aimed to investigate how reactive oxygen species (ROS), a frequent by-product of radiotherapy and temozolomide chemotherapy, regulate PP2A function via its methylesterase PME-1, and how PME-1 overexpression impacts the response of GBM cells to oxidative stress. We found that in two glioblastoma cell lines, U87MG and U251MG, expression of PME-1 is positively correlated with the sensitivity of the cells to H
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Registered trials
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