ArticleFuture science OA2026
USP14 promotes head and neck squamous cell carcinoma progression via deubiquitinating and stabilizing CFL2.
Article in Future science OA, 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
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
aimTo identify novel substrates of USP14 and elucidate the molecular mechanisms by which USP14 promotes head and neck squamous cell carcinoma (HNSCC) progression. MATERIALS AND
methodsUSP14 expression patterns were examined in HNSCC tissues and cell lines. Functional effects were assessed using genetic knockout and overexpression models
resultsUSP14 was significantly overexpressed in HNSCC and correlated with poor prognosis. Genetic knockout of USP14 markedly suppressed HNSCC cell proliferation, migration, and tumor growth, while USP14 overexpression exerted opposite effects. Mechanistically, we identified CFL2 as a novel substrate of USP14; USP14 directly interacted with and deubiquitinated CFL2, thereby enhancing its stability by preventing proteasomal degradation. Clinically, CFL2 was also overexpressed in HNSCC and its elevated levels correlated with reduced overall survival. Functionally, CFL2 overexpression significantly rescued the anti-tumor effects of USP14 knockout, including impaired cell proliferation and migration.
conclusionIn summary, our findings identify a novel USP14-CFL2 regulatory axis and establish USP14 as a critical promoter of HNSCC progression, acting through CFL2 deubiquitination and stabilization.
Indexed as
Identifiers
What Socratic 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 Socratic graph.