ArticleCancer letters2025
Anti-tumor activity of CDYL2b in prostate cancer.
Article in Cancer letters, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
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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
2 citing papers in PubMed.
- Promotion of breast cancer by the DNPH1 enzyme.iScience · 2026Article
- Structural landscape of H3K27me3 recognition by protein domains and their potential for inhibition.The Journal of biological chemistry · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors.
Funding
Abstract
Prostate cancer is a leading cause of death among men, yet the molecular underpinnings of this malignancy are still not fully understood. We discovered that two histone demethylases driving prostate tumorigenesis, the JMJD2A and JMJD2B enzymes, suppressed transcription of the CDYL2 epigenetic reader gene. Bioinformatic analyses showed that low CDYL2 expression in prostate tumors was associated with more metastasis and disease recurrence as well as reduced survival. Out of the four predicted CDYL2 isoforms, all of which were capable of forming homo- and heteromers, only CDYL2b was appreciably expressed in prostate cancer cells and tightly associated with chromatin. Overexpression of CDYL2b in human DU145 and 22Rv1 prostate cancer cells decreased their growth and clonogenic activity in vitro as well as tumor expansion in nude mice, while CDYL2b downregulation stimulated LNCaP cell growth. RNA sequencing exposed that CDYL2b induced upregulation of transcription factor genes HES7, KLF17 and TBX6 and overexpression of those factors phenocopied to various degrees the anti-oncogenic effects of CDYL2b. Further JMJD2B, but not JMJD2A, robustly formed complexes with CDYL2b and antagonized CDYL2b in upregulating HES7 transcription. In conclusion, our data highlight that CDYL2b can suppress prostate tumorigenesis, while JMJD2A and JMJD2B may exert their pro-oncogenic functions in part through stifling CDYL2b transcription or CDYL2b activity. In addition, our study revealed that the developmental transcription factors TBX6 and HES7 may also suppress tumorigenesis.
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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.