ArticleCell reports2025
CDH3-AS1 antisense RNA enhances P-cadherin translation and acts as a tumor suppressor in melanoma.
Article in Cell reports, 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.
- Dysregulation of the PATZ1/CTCF Balance Silences ZBTB20 to Drive Melanoma Progression.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- CDH3 in human tumors: tumor biology and potential therapeutic target.Frontiers in pharmacology · 2026Review
Corrections and comments
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Authors and funding
10 authors.
Funding
Abstract
Thousands of regulatory non-coding RNAs (ncRNAs) have been annotated, yet their roles in gene regulation and cancer progression remain unclear. Mapping the landscape of ncRNA expression during melanoma progression revealed that ncRNAs represented nearly half of the deregulated genes, with antisense RNAs (asRNAs) comprising a large portion. CDH3-AS1, the most downregulated asRNA, overlaps the CDH3 gene, which encodes P-cadherin, a key cell adhesion protein that is reduced in melanoma. Overexpression of CDH3-AS1 increased cell aggregation and reduced xenograft tumor growth, mimicking the effects of CDH3. CDH3-AS1 interacted with CDH3 mRNA, increased ribosome occupancy, and enhanced P-cadherin translation through a mechanism resembling SINEB2 sequence to up-regulate translation (SINEUP)-mediated translational control. asRNAs complementary to 5' UTRs generally increase the ribosome occupancy of their cognate mRNAs, suggesting broader translational control through this mechanism. This study revealed CDH3-AS1-mediated enhancement of P-cadherin translation as a tumor-suppressive axis in melanoma and highlighted the broader potential of asRNAs as regulators of protein translation.
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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.