ArticleCancer cell international2026
Inhibition of RBM23 induces ferroptosis in colon cancer cells via c-Myc regulation.
Article in Cancer cell international, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
backgroundRNA binding motif protein 23 (RBM23) is a member of the RNA binding motif gene family, functioning as a transcriptional cofactor and pre-mRNA splicing factor. While RBM23 is known to activate the NF-κB pathway in hepatocellular carcinoma, its role in other cancers remains unclear. In this study, we report for the first time that RBM23 inhibition induces ferroptosis via c-Myc regulation in colon cancer cells.
methodsRBM23 overexpression in CRC was assessed using qRT-PCR and Western blotting. Functional assays, including CCK-8 and colony formation, were conducted to examine cell viability. To investigate the regulatory role of RBM23 in c-Myc expression, siRNA knockdown was followed by nuclear fractionation, cycloheximide chase, and serum stimulation assays. Immunofluorescence confirmed subcellular localization. RBM23’s role in glucose metabolism was analyzed through qRT-PCR, Western blotting, and glucose uptake assays. Oxidative stress and ferroptosis were evaluated using C11-BODIPY, DCFH-DA staining, and Western blotting. Bioinformatic analyses supported experimental data.
resultsRBM23 knockdown significantly reduced c-Myc protein levels and stability. This led to decreased expression of glycolytic enzymes and impaired glucose uptake. As a result, metabolic suppression triggered oxidative stress, which was further amplified by c-Myc deficiency. Elevated ROS levels regulated the expression of ferroptosis-related factors such as GPX4 and KEAP1, leading to ferroptotic cell death. These findings suggest that RBM23 maintains metabolic homeostasis and cell survival through c-Myc stabilization.
conclusionsRBM23 inhibits ferroptosis in CRC cells by regulating c-Myc-mediated metabolic pathways. Our findings suggest that RBM23 serves as a potential biomarker and therapeutic target in colorectal cancer.
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