ArticleMolecular and cellular biochemistry2025
ZFP36L1 and ZFP36L2 reduce cyclin D1 expression by decreasing expression of E2F1 and long 3'UTR isoform of CCND1 transcripts.
Article in Molecular and cellular biochemistry, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed.
- Zinc finger proteins (ZFPs) in health and disease.Molecular biomedicine · 2026Review
- Variable roles of miRNA- and apoptosis-linked genes in invasive breast cancer: expression patterns, clinicopathological associations, and prognostic significance.Molecular biology reports · 2025Article
- Integrative RNA-seq and CLIP-seq analysis revealsFrontiers in physiology · 2025Article
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Authors and funding
6 authors.
Funding
Abstract
The CCND1 mRNA possesses at least two distinct lengths of the 3'-untranslated region (3'UTR), with the long isoform containing multiple AU-rich elements (AREs). The tandem zinc finger (TZF) domains of human ZFP36 family members have the capacity to bind to AREs and promote mRNA degradation. Our previous study demonstrated that mutations in the TZF domain of ZFP36L1 or ZFP36L2 increased the CCND1 expression. In this study, we investigated whether ZFP36L1 and ZFP36L2 could downregulate the expression of the long 3'UTR isoform of CCND1 mRNA in human colorectal cancer (CRC) cells. Firstly, the Gene Expression Profiling Interactive Analysis 2 database indicated downregulation of ZFP36 and ZFP36L1, while E2F1 and CCND1 were upregulated in human CRC tissues compared to normal colorectal tissues. Overexpression of ZFP36L1 and/or ZFP36L2 in T-REx-293, DLD-1, and HCT116 cells led to a decrease in the total CCND1, long isoform ratio of CCND1 mRNA, and E2F1 expression. Conversely, knockdown of ZFP36L1 and ZFP36L2 in HCT116 cells resulted in an increase in total CCND1, long isoform ratio of CCND1 mRNA, and E2F1 expression. Knockdown of E2F1 decreased CCND1 expression, indicating a potential role for E2F1 in regulating CCND1 expression at the transcriptional level. These findings suggest that ZFP36L1 and ZFP36L2 play a negative role in CCND1 expression. The underlying mechanisms might involve the reduction of E2F1 transactivation at the transcriptional level and the promotion of AREs-mediated decay of the long 3'UTR isoform of CCND1 through posttranscriptional processes.
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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 OpenQuestion graph.