ArticleOncogene2025
Non-classic deubiquitinase USP13 inhibits bladder cancer metastasis through destabilizing cytoplasmic KDM3A.
Article in Oncogene, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. 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
- Retraction · 2025-07-30Concerns/Issues about Data · Concerns/Issues about Image · Duplication of/in Image · Error in Image · Euphemisms for Duplication · Investigation by Journal/Publisher · Objections by Author(s) · Unreliable Data · · See also: https://pubpeer.com/publications/DD9219B079B24221281283A08A22EC
- Retracted
Authors and funding
16 authors.
Funding
Abstract
Bladder cancer (BLCa) metastasis is a predominant cause of death for bladder cancer patients. Histone demethylase KDM3A specifically removes the repressive mono- or di-methyl marks from H3K9 and thus contributes to the activation of gene transcription. However, the underlying mechanisms of KDM3A in bladder cancer are poorly understood. Here, we report that high levels of KDM3A are associated with bladder cancer clinical progression. KDM3A silencing inhibits bladder cancer cell growth, cell migration and invasion in vitro and in vivo. Mechanistically, we identify that non-classic deubiquitinase USP13 interacts with KDM3A to promote its degradation in cytoplasm via the proteasome-specific pathway. USP13 was significantly down-regulated in bladder cancer tissues and negatively associated with KDM3A expression. Furthermore, we show in bladder injected-liver metastasis xenograft model that USP13 inhibits bladder cancer metastasis through destabilizing cytoplasmic KDM3A. Collectively, our findings identify KDM3A is an important regulator of bladder cancer cell growth and metastasis and targeting USP13/KDM3A complex could be a valuable strategy to ameliorate bladder cancer progression and metastasis.
Indexed as
Identifiers
40253486What 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.