ArticleCancer gene therapy2023
c-Myc-induced long noncoding RNA MIRE cooperates with hnRNPK to stabilize ELF2 mRNA and promotes clear cell renal cell carcinogenesis.
Article in Cancer gene therapy, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 7 citations in OpenAlex.
- Long Non-Coding RNAs in Pathogenesis of Renal Cell Carcinoma: Epigenetic Regulation, Signaling Pathways, and Therapeutic Strategies.International journal of molecular sciences · 2026Review
- TRIM21-Mediated ubiquitination of FBL suppresses PI3K/AKT signaling and tumor progression in clear cell renal cell carcinoma.Cellular and molecular life sciences : CMLS · 2026Article
- Phase separation paints Xi with Xist.Cell research · 2025Article
- ETS-1 in tumor immunology: implications for novel anti-cancer strategies.Frontiers in immunology · 2025Review
- Comprehensive analysis of E47‑like factors and verification of ELF4 in clear cell renal cell carcinoma.Oncology letters · 2023Article
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
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Abstract
Elevated expression of c-Myc is associated with a variety of human cancers including clear cell renal cell carcinoma (ccRCC). Increasing evidence suggests that long noncoding RNAs (lncRNAs) are an important class of molecules that regulate both tumor initiation and progression. Here, we report the lncRNA c-Myc-induced regulator of ELF2 (MIRE) as a transcriptional target of c-Myc. MIRE functions as an oncogenic molecule in ccRCC by increasing ELF2 expression. Mechanistically, MIRE promotes phase separation of the RNA binding protein hnRNPK and facilitates the binding of hnRNPK to ELF2 mRNA, thereby resulting in the stabilization of ELF2 mRNA. Interestingly, MIRE is also under transcriptional control by ELF2, establishing an ELF2-MIRE positive feedback loop. Together, these findings provide new insights into the mechanisms by which c-Myc promotes tumorigenesis. They also implicate MIRE as an important regulator of ccRCC carcinogenesis.
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Registered trials
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