ArticleNucleic acids research2015
Splicing of a non-coding antisense transcript controls LEF1 gene expression.
Article in Nucleic acids research, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 8 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.
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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.
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Who cites it
8 citing papers in PubMed, 11 citations in OpenAlex.
- Aging-associated DNA methylation of LEF1 modulates inflammation and neurodegenerative pathways.Frontiers in immunology · 2025Article
- Autoregulation of JARID2 through PRC2 interaction with its antisense ncRNA.BMC research notes · 2020Article
- Novel Non-Coding Transcript inFrontiers in oncology · 2020Article
- LEF1-AS1, long non-coding RNA, inhibits proliferation in myeloid malignancy.Journal of cellular and molecular medicine · 2019Article
- Wnt signaling pathway protein LEF1 in cancer, as a biomarker for prognosis and a target for treatment.American journal of cancer research · 2017Review
- Antisense non-coding RNAs and regulation of gene transcription.Transcription · 2016Article
- Characteristics of Antisense Transcript Promoters and the Regulation of Their Activity.International journal of molecular sciences · 2015Review
- Article
Corrections and comments
- Erratum issued
Authors and funding
9 authors at 3 institutions in 2 countries.
Funding
Abstract
In this report we have analyzed the role of antisense transcription in the control of LEF1 transcription factor expression. A natural antisense transcript (NAT) is transcribed from a promoter present in the first intron of LEF1 gene and undergoes splicing in mesenchymal cells. Although this locus is silent in epithelial cells, and neither NAT transcript nor LEF1 mRNA are expressed, in cell lines with an intermediate epithelial-mesenchymal phenotype presenting low LEF1 expression, the NAT is synthesized and remains unprocessed. Contrarily to the spliced NAT, this unspliced NAT down-regulates the main LEF1 promoter activity and attenuates LEF1 mRNA transcription. Unspliced LEF1 NAT interacts with LEF1 promoter and facilitates PRC2 binding to the LEF1 promoter and trimethylation of lysine 27 in histone 3. Expression of the spliced form of LEF1 NAT in trans prevents the action of unspliced NAT by competing for interaction with the promoter. Thus, these results indicate that LEF1 gene expression is attenuated by an antisense non-coding RNA and that this NAT function is regulated by the balance between its spliced and unspliced forms.
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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.