ArticleTranslational oncology2026
UCHL1 promotes temozolomide resistance in glioblastoma by inhibiting the ubiquitination-mediated degradation of keratin 8.
Article in Translational 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
10 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundResistance to temozolomide (TMZ)-based chemotherapy is a major cause of progression and recurrence in patients with glioblastoma. Although the deubiquitinating enzyme ubiquitin C-terminal hydrolase L1 (UCHL1) has been implicated in tumor chemoresistance, its roles and underlying mechanisms in TMZ resistance remain unclear.
methodsBioinformatics analyses and immunohistochemistry were used to assess the prognostic significance and the levels of UCHL1 in glioma specimens. Co-immunoprecipitation assays and mass spectrometry were performed to identify protein interactors of UCHL1. The impact of the UCHL1-Keratin 8 (KRT8) axis on TMZ resistance was evaluated using the cell counting kit-8 (CCK-8) assay and western blotting.
resultsWe found that UCHL1 induced resistance of glioblastoma cells to TMZ. Moreover, UCHL1 expression was significantly upregulated in patients with TMZ-resistant glioma and correlated with poor prognosis. As a deubiquitinase belonging to the UCH enzyme family, UCHL1 utilizes its deubiquitination activity to remove K27-linked polyubiquitin chains from KRT8, thereby preventing KRT8 degradation by the proteasome and maintaining its stability. In vitro assays further demonstrated that depletion of the UCHL1-KRT8 axis weakened chemoresistance by increasing TMZ-induced apoptosis.
conclusionThese findings reveal a novel signaling axis underlying TMZ resistance in glioblastoma and highlight the UCHL1-KRT8 axis as a promising therapeutic target.
Indexed as
Identifiers
What 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.