ArticleHeliyon2024
The RNA m6A writer RBM15 contributes to the progression of esophageal squamous cell carcinoma by regulating miR-3605-5p/KRT4 pathway.
Article in Heliyon, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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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.
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Who cites it
7 citing papers in PubMed, 6 citations in OpenAlex.
- RBM protein family: Focusing on the occurrence, progression and treatment of cancer.Medical oncology (Northwood, London, England) · 2026Review
- RBM15 in diseases: Molecular mechanisms and clinical opportunities from RNA mGenes & diseases · 2026Review
- mFrontiers in cell and developmental biology · 2026Review
- Role of N6-methyladenosine methyltransferase component RBM15 in cancer progression and its therapeutic potential.Discover oncology · 2025Review
- Mirtrons in Human Cancers.Onco · 2025Article
- RBM15-mediated mFrontiers in cell and developmental biology · 2025Review
- The role of N(6)-methyladenosine (m6a) modification in cancer: recent advances and future directions.EXCLI journal · 2025Review
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Authors and funding
1 author at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cancer progression can be modulated by N6-methyladenosine (m6A) modification. RNA binding motif protein 15 (RBM15) is an essential RNA m6A writer that influences carcinogenesis, however its significance in esophageal squamous cell carcinoma (ESCC) is uncertain. This research is intended to examine how RBM15 regulates the development of ESCC. We performed qRT-PCR analysis to evaluate the expression of RBM15, microRNA (miR-3605-5p) as well as keratin 4 (KRT4) in ESCC. Target relationship between miR-3605-5p and KRT4 was validated by dual luciferase reporter assay. Western blotting analyzed the protein levels of KRT4, p53, and p21. To demonstrate that RBM15 is responsible for the m6A alteration of miR-3605-5p, RIP and Me-RIP experiments were carried out concurrently. m6A content was measured by m6A quantification assay. Cell growth and migration were assessed using the CCK-8 and transwell assays. In addition, the role of RBM15 in vivo was examined using a mouse tumor xenograft model. RBM15 and miR-3605-5p were both substantially expressed in ESCC, however KRT4 was not expressed highly. Overexpressed RBM15 triggered cell proliferation and migration in ESCC. Besides, RBM15/m6A could mediate pri-3605-5p to form the mature miR-3605-5p, and miR-3605-5p further targeted KRT4. Further investigations showed that upregulation of KRT4 overturned the promoting impact of RBM15 overexpression on cell proliferation as well as on cell migration in ESCC by activating p53 signaling pathway. This work implied the carcinogenic activity of RBM15/m6A in ESCC via miR-3605-5p/KRT4 pathway, providing a novel m6A modification pattern in the tumorigenesis of ESCC.
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