ArticleBritish journal of cancer2024
SON is an essential RNA splicing factor promoting ErbB2 and ErbB3 expression in breast cancer.
Article in British journal of cancer, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed.
- Targeting Osteoporosis-Osteoarthritis Comorbidity: Multi-Omics Identification of SON and Exploration of Therapeutic Agents.International journal of molecular sciences · 2026Article
- G-patch proteins: important regulators of pre-mRNA splicing and ribosome biogenesis.Frontiers in cell and developmental biology · 2026Review
- Toward unraveling molecular grammars for dsRNA-binding proteins: substrate recognition to binding mechanisms.BMB reports · 2025Review
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Authors and funding
16 authors.
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Abstract
backgroundIn breast cancer, ErbB receptors play a critical role, and overcoming drug resistance remains a major challenge in the clinic. However, intricate regulatory mechanisms of ErbB family genes are poorly understood. Here, we demonstrate SON as an ErbB-regulatory splicing factor and a novel therapeutic target for ErbB-positive breast cancer.
methodsSON and ErbB expression analyses using public database, patient tissue microarray, and cell lines were performed. SON knockdown assessed its impact on cell proliferation, apoptosis, kinase phosphorylation, RNA splicing, and in vivo tumour growth. RNA immunoprecipitation was performed to measure SON binding.
resultsSON is highly expressed in ErbB2-positive breast cancer patient samples, inversely correlating with patient survival. SON knockdown induced intron retention in selective splice sites within ErbB2 and ErbB3 transcripts, impairing effective RNA splicing and reducing protein expression. SON disruption suppressed downstream kinase signalling of ErbB2/3, including the Akt, p38, and JNK pathways, with increased vulnerability in ErbB2-positive breast cancer cells compared to ErbB2-negative cells. SON silencing in ErbB2-positive breast cancer xenografts led to tumour regression in vivo.
conclusionWe identified SON as a novel RNA splicing factor that plays a critical role in regulating ErbB2/3 expression, suggesting SON is an ideal therapeutic target in ErbB2-positive breast cancers.
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