ArticleCell death discovery2025
m6A-modified LINC02418 induces transcriptional and post-transcriptional modification of CTNNB1 via interacting with YBX1 and IGF2BP1 in colorectal cancer.
Article in Cell death discovery, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
What it found
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Who cites it
9 citing papers in PubMed.
- Programmable ZBTB7A RNA NMolecular cancer · 2026Article
- SDCBP Cooperates With YBX1 to Promote ESCC Metastasis by Forming a Positive Feedback Loop With Wnt-β-Catenin Signaling Pathway.Journal of biochemical and molecular toxicology · 2026Article
- RNA Regulatory Networks: Key Hubs in the Panorama of Cancer and Emerging Therapeutic Targets.MedComm · 2026Review
- Inhibition of radiotherapy sensitivity in nasopharyngeal carcinoma via the long non-coding RNATranslational cancer research · 2026Article
- RM2Target v2.0: an updated database for the target genes of writers, erasers, and readers of RNA modifications.Nucleic acids research · 2026Article
- YBX1 as an adaptive RNA hub in cancer: linking state-dependent RNA regulation to tumor immunity, metabolic reprogramming, and therapy resistance.Frontiers in immunology · 2026Review
- The Central Role of m6A as Epigenetic Regulator in Metabolic Disorders of Therapeutic Potential and Clinical Implications.Molecular neurobiology · 2025Review
- Multifaceted functions of Y‑box binding protein 1 in RNA methylated modifications (Review).Molecular medicine reports · 2025Review
- METTL3 in colorectal cancer: molecular insights and clinical implications.Molecular biology reports · 2025Review
Corrections and comments
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Authors and funding
9 authors.
Funding
Abstract
Colorectal cancer (CRC) represents a significant menace to human health, but its molecular pathogenesis remains unclear. Herein, we explored the functional role of LINC02418 in CRC progression. The function of LINC02418 in CRC was determined through vitro and in vivo experiments. The molecular mechanism of LINC02418 in CRC was explored by quantitative real-time PCR (qPCR) analyses, western blot, luciferase reporter assay, methylated RNA immunoprecipitation (MeRIP) assay, RNA pull-down, RNA immunoprecipitation (RIP) assay and chromatin immunoprecipitation (ChIP) assay. The results revealed that LINC02418 expression was upregulated in CRC tissues and the high expression of LINC02418 was related to unfavorable survival of CRC patients. Besides, knockdown of LINC02418 expression resulted in the inhibition of proliferation and metastasis of CRC cells in vitro and in vivo. Mechanistically, we found METTL3-mediated m6A modification induced the aberrant expression of LINC02418 in CRC. LINC02418 could interact with YBX1 and enhance YBX1 DNA-binding ability to the CTNNB1 promoter, resulting in transcriptional activation of CTNNB1. In the post-transcriptional stage, LINC02418 could also enhance CTNNB1 stability by promoting the interaction between IGF2BP1 protein and CTNNB1 mRNA. What is more, LINC02418 expression could be transcriptionally enhanced by YBX1 protein. Collectively, this study unveils a novel oncogenic mechanism for LINC02418 in CRC and the LINC02418 might be a novel therapeutic target in CRC treatment.
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Registered trials
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