ArticleCancer reports (Hoboken, N.J.)2025
RALYL Overexpression Suppresses Colorectal Cancer via Modulating HNRNPC-Mediated MNK2 Alternative Splicing.
Article in Cancer reports (Hoboken, N.J.), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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Who cites it
2 citing papers in PubMed.
- Alternative splicing factor RAB3IP as a novel risk signature to predict the prognosis of colorectal cancer.Journal of Cancer · 2025Article
- Single-Cell RNA-Seq Recognized Key Genes for Metastasis and Macrophage Infiltration in Colorectal Cancer.Human mutation · 2025Article
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9 authors.
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Abstract
backgroundColorectal cancer (CRC) stands as the second most prevalent cause of cancer-related mortality globally, while its incidence holds the third position among newly diagnosed cancer cases worldwide. Colorectal carcinogenesis is complicated, and the processes are triggered by the complex interaction of some genetic and environmental factors, including DNA methylation. Previous studies showed that RALYL is hypermethylated in CRC. We aimed to explore the role of RALYL in CRC involved in MNK2 alternative splicing in the present study.
methodsBioinformatics analysis, detection in CRC samples, and experiments in vitro and in vivo combined with gene knockdown and overexpression were conducted. Cell proliferation and tumor growth assays were performed.
resultsResults showed that hypermethylated RALYL is lowly expressed in CRC. Overexpression of RALYL suppresses cell proliferation in vitro and tumor growth in vivo in CRC. MNK2 alternative splicing is essential for the tumor suppressive role of RALYL, along with RALYL regulating MNK2 alternative splicing via HNRNPC in CRC.
conclusionsRALYL potentially exerts an inhibitory effect on CRC by engaging with HNRNPC to orchestrate the alternative splicing of MNK2. RALYL binds to HNRNPC to promote MNK2 splicing into MNK2a instead of MNK2b, consequently activating the p38 MAPK signaling pathway and inhibiting tumor proliferation in CRC. Our findings suggest that RALYL might suppress CRC through binding to HNRNPC to promote MNK2 splicing toward MNK2a, thereby activating the p38 MAPK signaling cascade.
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