ArticleCytoJournal2026
Ubiquitin-specific protease 5 promotes breast cancer progression by stabilizing Forkhead box M1 through deubiquitination.
Article in CytoJournal, 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
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Objective: Breast cancer continues to be a leading and aggressive cancer in women. Despite improvements in early treatment, challenges such as rapid tumor proliferation, metastasis, and drug resistance persist. This research examines how the deubiquitinase ubiquitin-specific protease 5 (USP5) maintains Forkhead box M1 (FOXM1) protein stability and its impact on the advancement of breast cancer. Material and Methods: Data from The Cancer Genome Atlas were utilized to investigate the expression patterns and interactions of USP5 and FOXM1 in breast cancer. The breast cancer cell lines were subjected to functional testing, including invasion, migration, and proliferation. The expression and interaction of USP5 and FOXM1 were examined using quantitative real-time polymerase chain reaction, Western blot, and co-immunoprecipitation analyses. Protein stability and ubiquitination assays were performed to evaluate the effect of USP5 on FOXM1 stability. Results: USP5 stabilized the FOXM1 protein by deubiquitination. Overexpression of USP5 increased FOXM1 levels, while USP5 knockdown accelerated FOXM1 degradation. The deubiquitinating enzyme USP5 inhibited the proteasomal degradation of FOXM1, enhancing its stability. Functional assays showed that USP5 overexpression promoted breast cancer cell progression, while USP5 knockdown inhibited these malignant phenotypes. Conclusion: USP5 enhances breast cancer progression by stabilizing FOXM1 through deubiquitination.
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.