ArticleJournal of neuro-oncology2026
Pharmacological transglutaminase 2 inhibition enhances temozolomide response in patient-derived glioblastoma tumorspheres.
Article in Journal of neuro-oncology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
13 authors.
Funding
Abstract
purposeGlioblastoma (GBM) is the most common and aggressive primary malignant brain tumor, with a median survival of less than two years despite standard therapy. Transglutaminase 2 (TGM2) contributes to tumor progression and poor clinical outcomes. This study evaluated the therapeutic potential of combining streptonigrin (SN), a TGM2 inhibitor, with temozolomide (TMZ), the standard chemotherapeutic agent for GBM.
methodsTwo patient-derived GBM tumorspheres (TSs; TS15-88, proneural subtype; TS19-156, classical subtype) were treated with SN, TMZ, or their combination. Cell viability and ATP production were measured to assess cell proliferation, and synergy was quantified using the Bliss synergy score. Apoptosis was analyzed by flow cytometry. Stemness and invasiveness were evaluated using neurosphere formation and three-dimensional invasion assays. Protein and mRNA expression levels were assessed by western blotting and RNA sequencing. In vivo efficacy was evaluated using a mouse orthotopic xenograft model.
resultsThe combination of SN and TMZ significantly reduced cell viability and ATP levels and induced apoptosis more effectively than either agent alone. Moreover, combination treatment effectively reduced stemness and invasiveness in GBM TSs, along with the expression of related proteins and mRNAs. In vivo, combination therapy prolonged survival in mice and reduced the expression of invasion-related proteins, as demonstrated by immunohistochemistry.
conclusionThese findings suggest that targeting TGM2 with SN enhances the therapeutic efficacy of TMZ in GBM. The combination of SN and TMZ may represent one potential therapeutic approach for GBM and warrants further mechanistic and translational investigation.
Indexed as
Identifiers
41483361What OpenQuestion holds
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.