ArticleCell & bioscience2018
Long non-coding RNA CASC15 promotes melanoma progression by epigenetically regulating PDCD4.
Article in Cell & bioscience, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 34 papers, 1 of them a synthesis that pooled it.
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.
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Who cites it
34 citing papers in PubMed, 1 synthesis or guideline pooled it, 56 citations in OpenAlex.
- A study of the prognostic value of long non-coding RNA CASC15 in human solid tumors utilizing The Cancer Genome Atlas (TCGA) datasets and a meta-analysis.Clinical and experimental medicine · 2023Pooled it
- Article
- Unravelling the Regulatory Roles of lncRNAs in Melanoma: From Mechanistic Insights to Target Selection.International journal of molecular sciences · 2025Review
- YY1-induced lncRNA00511 promotes melanoma progression via the miR-150-5p/ADAM19 axis.American journal of cancer research · 2024Article
- lncRNAs-EZH2 interaction as promising therapeutic target in cutaneous melanoma.Frontiers in molecular biosciences · 2023Review
- Pathogenic roles of long noncoding RNAs in melanoma: Implications in diagnosis and therapies.Genes & diseases · 2023Review
- Identification of endoplasmic reticulum stress-related lncRNAs in lung adenocarcinoma by bioinformatics and experimental validation.Annals of medicine · 2023Article
- Review
- Review
- Whole-genome-scale identification of novel non-protein-coding RNAs controlling cell proliferation and survival through a functional forward genetics strategy.Scientific reports · 2022Article
- LncRNA CASC15, MiR-23b Cluster and SMAD3 form a Novel Positive Feedback Loop to promote Epithelial-Mesenchymal Transition and Metastasis in Ovarian Cancer.International journal of biological sciences · 2022Article
- Regulation of melanoma malignancy by the RP11-705C15.3/miR-145-5p/NRAS/MAPK signaling axis.Cancer gene therapy · 2021Article
- STAT3-induced ZBED3-AS1 promotes the malignant phenotypes of melanoma cells by activating PI3K/AKT signaling pathway.RNA biology · 2021Article
- Review
- The Functional Role of Long Non-Coding RNAs in Melanoma.Cancers · 2021Review
- Circ_0003266 sponges miR-503-5p to suppress colorectal cancer progression via regulating PDCD4 expression.BMC cancer · 2021Observational
- Clinical Significance of PDCD4 in Melanoma by Subcellular Expression and in Tumor-Associated Immune Cells.Cancers · 2021Article
- Article
- Comprehensive Review on the Clinical Relevance of Long Non-Coding RNAs in Cutaneous Melanoma.International journal of molecular sciences · 2021Review
- Functional Prediction of Long Noncoding RNAs in Cutaneous Melanoma Using a Systems Biology Approach.Bioinformatics and biology insights · 2021Article
Corrections and comments
- Retracted
Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundLong non-coding RNAs (LncRNAs) have been identified as critical regulators in a variety of cancer types. Cancer susceptibility candidate 15 (CASC15), a lncRNA located at chromosome 6p22.3, has been discovered to participate in melanoma progression and phenotype switching. Nevertheless, the roles and molecular mechanisms of CASC15 in melanoma are far from being understood.
resultsWe found that CASC15 expression was up-regulated in melanoma tissues and associated with advanced pathological stages. Function experiments displayed that CASC15 knockdown hindered proliferation, facilitated apoptosis and suppressed invasion, while CASC15 overexpression facilitated proliferation and invasion in melanoma cells. Further mechanistic analysis showed that CASC15 epigenetically silenced the expression of programmed cell death 4 (PDCD4) by recruiting EZH2 and increasing H3K27me3 level at the promoter region of PDCD4. Additionally, PDCD4 overexpression inhibited proliferation, enhanced apoptosis and decreased invasion of melanoma cells. Moreover, CASC15-knockdown-induced anti-cancer effects were abated by PDCD4 down-regulation. Furthermore, depletion of CASC15 blocked tumor growth of melanoma by up-regulating PDCD4 in vivo.
conclusionsCASC15 acts as an oncogene by negatively regulating PDCD4 expression via recruiting EZH2 and subsequently increasing H3K27me3 level. Together, our study indicates that CASC15/EZH2/PDCD4 may serve as a promising therapeutic target for melanoma intervention.
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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 Socratic graph.