ArticlePeerJ2022
RNA-binding protein CELF6 modulates transcription and splicing levels of genes associated with tumorigenesis in lung cancer A549 cells.
Article in PeerJ, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers, 1 of them a synthesis that pooled it.
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Who cites it
9 citing papers in PubMed, 1 synthesis or guideline pooled it, 11 citations in OpenAlex.
- tRNA-derived fragments: mechanism of gene regulation and clinical application in lung cancer.Cellular oncology (Dordrecht, Netherlands) · 2024Pooled it
- CELF family of RNA-binding proteins: roles in disease biology and potential for therapeutic intervention.Cell communication and signaling : CCS · 2026Review
- PDPK1 activates BIRC3 via NFKB1 to promote radiotherapy resistance in lung adenocarcinoma.Cancer cell international · 2026Article
- MDM2 promotes CELF6 ubiquitination-dependent degradation to promote neuroblastoma cell proliferation.Cell death & disease · 2025Article
- The role of RNA binding proteins in cancer biology: A focus on FMRP.Genes & diseases · 2025Review
- RNA-binding proteins and autophagy in lung cancer: mechanistic insights and therapeutic perspectives.Discover oncology · 2025Review
- CELF1 Promotes Post-myocardial Infarction Cardiac Remodeling Via Suppression of FMO2.Cardiovascular toxicology · 2025Article
- Long noncoding RNA LINC01594 inhibits the CELF6-mediated splicing of oncogenic CD44 variants to promote colorectal cancer metastasis.Cell death & disease · 2023Article
- Role of the RNA-binding protein family in gynecologic cancers.American journal of cancer research · 2023Review
Corrections and comments
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Authors and funding
10 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
CELF6 (CUGBP Elav-Like Family Member 6), a canonical RNA binding protein (RBP), plays important roles in post-transcriptional regulation of pre-mRNAs. However, the underlying mechanism of lower expressed CELF6 in lung cancer tissues is still unclear. In this study, we increased CELF6 manually in lung cancer cell line (A549) and utilized transcriptome sequencing (RNA-seq) technology to screen out differentially expressed genes (DEGs) and alternative splicing events (ASEs) after CELF6 over-expression (CELF6-OE). We found that CELF6-OE induced 417 up-regulated and 1,351 down-regulated DEGs. Functional analysis of down-regulated DEGs showed that they were highly enriched in immune/inflammation response- related pathways and cell adhesion molecules (CAMs). We also found that CELF6 inhibited the expression of many immune-related genes, including TNFSF10, CCL5, JUNB, BIRC3, MLKL, PIK3R2, CCL20, STAT1, MYD88, and CFS1, which mainly promote tumorigenesis in lung cancer. The dysregulated DEGs were also validated by reverse transcriptase quantitative polymerase chain reaction (RT-qPCR) experiment. In addition, CELF6 regulates the splicing pattern of large number of genes that are enriched in p53 signaling pathway and apoptosis, including TP53 and CD44. In summary, we made an extensive analysis of the transcriptome profile of gene expression and alternative splicing by CELF6-OE, providing a global understanding of the target genes and underlying regulation mechanisms mediated by CELF6 in the pathogenesis and development of lung cancer.
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Registered trials
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