ArticleActa neuropathologica2019
RhoA regulates translation of the Nogo-A decoy SPARC in white matter-invading glioblastomas.
Article in Acta neuropathologica, 2019. 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, 9 citations in OpenAlex.
- Modern brachytherapy in glioblastoma: overcoming clinical barriers to improve local control.Frontiers in oncology · 2026Review
- Impact of glioma metabolism-related gene ALPK1 on tumor immune heterogeneity and the regulation of the TGF-β pathway.Frontiers in immunology · 2024Article
- Article
- Nogo-A/NgR signaling regulates stemness in cancer stem-like cells derived from U87MG glioblastoma cells.Oncology letters · 2022Article
- ENTPD5: identification of splicing variants and their impact on cancer survival.Purinergic signalling · 2021Article
Corrections and comments
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Authors and funding
23 authors at 8 institutions in 3 countries.
Funding
Abstract
Glioblastomas strongly invade the brain by infiltrating into the white matter along myelinated nerve fiber tracts even though the myelin protein Nogo-A prevents cell migration by activating inhibitory RhoA signaling. The mechanisms behind this long-known phenomenon remained elusive so far, precluding a targeted therapeutic intervention. This study demonstrates that the prevalent activation of AKT in gliomas increases the ER protein-folding capacity and enables tumor cells to utilize a side effect of RhoA activation: the perturbation of the IRE1α-mediated decay of SPARC mRNA. Once translation is initiated, glioblastoma cells rapidly secrete SPARC to block Nogo-A from inhibiting migration via RhoA. By advanced ultramicroscopy for studying single-cell invasion in whole, undissected mouse brains, we show that gliomas require SPARC for invading into white matter structures. SPARC depletion reduces tumor dissemination that significantly prolongs survival and improves response to cytostatic therapy. Our finding of a novel RhoA-IRE1 axis provides a druggable target for interfering with SPARC production and underscores its therapeutic value.
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Registered trials
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