ArticleHereditas2025
RBM15 promotes COAD progression by regulating the m6A modification of TMC5.
Article in Hereditas, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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
3 citing papers in PubMed.
- RBM15 transcription activated by EGR1 stimulates gastric cancer proliferation and metastasis by enhancing m6A modification of RREB1.Functional & integrative genomics · 2026Article
- RNA-binding motif proteins as context-dependent regulators of tumor-immune crosstalk, genome stability, and therapeutic vulnerabilities in cancer.Frontiers in immunology · 2026Review
- RBM15-mediated mFrontiers in cell and developmental biology · 2025Review
Corrections and comments
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Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundColon adenocarcinoma (COAD) is a frequent digestive system malignancy with high mortality and poor prognosis. Transmembrane Channel-like 5 (TMC5) has been reported to play an oncological role in various cancers. However, the role and mechanism of TMC5 in COAD remain unclear.
methodsTIMER and UALCAN databases analyzed the expression of TMC5 in COAD. TMC5, RNA-binding motif protein-15 (RBM15), E-cadherin, N-cadherin, Vimentin, Fibronectin, and RAD51 protein levels were determined using western blot. TMC5, RBM15, Ferritin heavy chain 1 (FTH1), and cystine/glutamate antiporter SLC7A11 (also commonly known as xCT) mRNA levels were examined using real-time quantitative polymerase chain reaction (RT-qPCR). Cell proliferation, apoptosis, migration, and invasion were assessed using 5-ethynyl-2'-deoxyuridine (EdU), flow cytometry, and transwell assays. Caspase 3 activity, ROS level, Fe
resultsTMC5 and RBM15 levels were significantly increased in COAD tissues and cells. Moreover, TMC5 silencing could inhibit COAD cell proliferation, migration, invasion, EMT, glycolysis, and induce apoptosis and ferroptosis in vitro, as well as repress tumor growth in vivo. At the molecular level, RBM15 could sustain RNA stability and TMC5 expression through regulating the m6Amodification.
conclusionRBM15 could facilitate COAD cell malignant behaviors at least by regulating the stability of TMC5 mRNA, providing a powerful and hopeful target for COAD treatment.
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