ArticleThe Prostate2022
AT-rich interaction domain 5A regulates the transcription of interleukin-6 gene in prostate cancer cells.
Article in The Prostate, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 21 citations in OpenAlex.
- CRISPR decodes the RNA regulatory network in prostate cancer: A review from mechanisms to precision therapeutics.Non-coding RNA research · 2026Review
- AT-rich interaction domain 5A facilitates axon regeneration through docking protein 6 in the peripheral nervous system.Burns & trauma · 2025Article
- Article
- AR coactivators, CBP/p300, are critical mediators of DNA repair in prostate cancer.bioRxiv : the preprint server for biology · 2024Article
- Novel prognostic gene signature for pancreatic ductal adenocarcinoma based on hypoxia.World journal of surgical oncology · 2023Article
- The uncharacterized transcriptOncotarget · 2023Article
- Recent Advances in the Role of Arid5a in Immune Diseases and Cancer.Frontiers in immunology · 2021Review
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
backgroundInterleukin-6 (IL-6) is a pleiotropic cytokine that confers androgen-independence and aggressiveness in prostate cancer (PCa); however, the molecular mechanisms regulating IL-6 expression remain unclear. The expression of ARID5A, an AT-rich interaction domain (ARID) DNA-binding motif-containing transcription factor is positively correlated with IL-6 expression in human PCa. We, therefore, hypothesized that ARID5A could regulate IL-6 expression in PCa.
methodsThe relationship between ARID5A and IL-6 in PCa patients was analyzed using statistical analyses of multiple clinical microarray data sets. To investigate whether ARID5A regulates IL-6 expression, CRISPR-driven ARID5A knockout clones were established in DU145 and PC-3 cells.
resultsAnalysis of three microarray data sets showed a positive correlation between ARID5A and IL-6 expression. The expression of IL-6 in ARID5A knockout clones was significantly reduced compared with control clones in both PCa cell lines. Knockout of ARID5A did not result in any loss of IL-6 mRNA stability. Instead, we observed a significant decrease in the occupancy of both active RNA Polymerase II and the active histone mark, H3K4me3 at the IL-6 transcriptional start site in ARID5A knockout PCa cells, suggesting a role for transcriptional regulation.
conclusionsOur study demonstrated that loss of ARID5A downregulates the expression of IL-6 at the transcriptional level.
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