ArticleArchives of medical science : AMS2025
Cyclin-dependent kinase 8/β-catenin signalling contributes to tumourigenesis in prostate cancer and can be regulated by miR-216a-5p.
Article in Archives of medical science : AMS, 2025. 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
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Introduction: Cyclin-dependent kinase 8 (CDK8), as an oncogene, contributes to carcinogenesis in several cancer types. However, the role of CDK8 in prostate cancer (PCa) has not been completely clarified. The present study was to investigate the molecular mechanisms underlying the progression of PCa. Material and methods: In human specimens, RT-qPCR and immunohistochemical (IHC) staining were used to detect the mRNA and protein expression of CDK8, respectively. Results: Up-regulation of CDK8 was observed in PCa tissues and associated with poor overall survival (OS) and disease-free survival (DFS). Knockdown of CDK8 by shRNA was able to repress cell proliferation and induce cell apoptosis in PC3 and DU145 cells, as well as reduce the protein expression of Wnt/β-catenin pathway components. CDK8 was a direct target of miR-216a-5p, and overexpression of CDK8 reduced the antineoplastic activities of miR-216a-5p Conclusions: miR-216a-5p/CDK8/β-catenin signalling cascade modulates the aggression of PCa. miR-216a-5p and CDK8, as promising therapeutic targets, might facilitate the development of therapeutic strategies for the treatment of PCa.
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.