ArticleCellular and molecular life sciences : CMLS2019
IGFBP-3 interacts with NONO and SFPQ in PARP-dependent DNA damage repair in triple-negative breast cancer.
Article in Cellular and molecular life sciences : CMLS, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 papers.
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Who cites it
58 citing papers in PubMed, 82 citations in OpenAlex.
- Multifaceted regulatory role of proline‑ and glutamine-rich splicing factor in tumors (Review).Molecular medicine reports · 2026Review
- IGFBP in tumor immunity: a novel target for cancer immunotherapy.Journal of translational medicine · 2026Review
- IGFBP3-SphK1/S1P Signaling Axis Drives Enzalutamide Resistance in Advanced Prostate Cancer.Molecular cancer therapeutics · 2026Article
- Targeting circSFPQ_008/SFPQ/BRCA1 axis for overcoming platinum resistance in ovarian cancer.MedScience · 2026Article
- A Functional Shift of IGFBP3 in Osteoarthritis: From Cartilage Protection to Disease Promotion.Journal of inflammation research · 2026Review
- LncRNAs as regulators of chemoresistance and chemosensitivity in triple-negative breast cancer.Genetics and molecular biology · 2026Article
- Targeting TDP1 phosphorylation by the natural product imperatorin promotes DNA repair and cardiac regeneration.Communications biology · 2025Article
- The multifaceted roles of ribosomal P complex in cancer.World journal of surgical oncology · 2025Review
- GPR81 nuclear transportation is critical for cancer growth and progression in lung and other solid cancers.World journal of clinical oncology · 2025Article
- In Vitro and In Silico Evaluation of the Potential Anti-Prostate Cancer Activity ofInternational journal of molecular sciences · 2025Article
- NONO interacts with nuclear PKM2 and directs histone H3 phosphorylation to promote triple-negative breast cancer metastasis.Journal of experimental & clinical cancer research : CR · 2025Article
- The mechanism of high mobility group box-1 in the proliferation and macrophage polarization in esophageal squamous cell carcinoma cells.European journal of medical research · 2025Article
- MCellular and molecular life sciences : CMLS · 2025Article
- CCCTC-binding factor regulates splicing factor proline and glutamine-rich to promote malignant growth of osteosarcoma.American journal of translational research · 2025Article
- Review
- A novel protein encoded by circCOPA inhibits the malignant phenotype of glioblastoma cells and increases their sensitivity to temozolomide by disrupting the NONO-SFPQ complex.Cell death & disease · 2024Article
- Established and Evolving Roles of the Multifunctional Non-POU Domain-Containing Octamer-Binding Protein (NonO) and Splicing Factor Proline- and Glutamine-Rich (SFPQ).Journal of developmental biology · 2024Review
- Epigenetic silencing ofEpigenomics · 2024Article
- Meta-analysis of RNA interaction profiles of RNA-binding protein using the RBPInper tool.Bioinformatics advances · 2024Article
- Signaling Pathways of the Insulin-like Growth Factor Binding Proteins.Endocrine reviews · 2023Article
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Authors and funding
5 authors at 1 institution in 2 countries.
Funding
Abstract
Women with triple-negative breast cancer (TNBC) are generally treated by chemotherapy but their responsiveness may be blunted by DNA double-strand break (DSB) repair. We previously reported that IGFBP-3 forms nuclear complexes with EGFR and DNA-dependent protein kinase (DNA-PKcs) to modulate DSB repair by non-homologous end-joining (NHEJ) in TNBC cells. To discover IGFBP-3 binding partners involved in chemoresistance through stimulation of DSB repair, we analyzed the IGFBP-3 interactome by LC-MS/MS and confirmed interactions by coimmunoprecipitation and proximity ligation assay. Functional effects were demonstrated by DNA end-joining in vitro and measurement of γH2AX foci. In response to 20 µM etoposide, the DNA/RNA-binding protein, non-POU domain-containing octamer-binding protein (NONO) and its dimerization partner splicing factor, proline/glutamine-rich (SFPQ) formed complexes with IGFBP-3, demonstrated in basal-like TNBC cell lines HCC1806 and MDA-MB-468. NONO binding to IGFBP-3 was also shown in a cell-free biochemical assay. IGFBP-3 complexes with NONO and SFPQ were blocked by inhibiting EGFR with gefitinib or DNA-PKcs with NU7026, and by the PARP inhibitors veliparib and olaparib, which also reduced DNA end-joining activity and delayed the resolution of the γH2AX signal (i.e. inhibited DNA DSB repair). Downregulation of the long noncoding RNA in NHEJ pathway 1 (LINP1) by siRNA also blocked IGFBP-3 interaction with NONO-SFPQ. These findings suggest a PARP-dependent role for NONO and SFPQ in IGFBP-3-dependent DSB repair and the involvement of LINP1 in the complex formation. We propose that targeting of the DNA repair function of IGFBP-3 may enhance chemosensitivity in basal-like TNBC, thus improving patient outcomes.
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