ArticleHereditas2025
RBM15 enhances paclitaxel resistance in triple-negative breast cancer by targeting m
Article in Hereditas, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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The trial behind it
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Who cites it
10 citing papers in PubMed.
- RBM protein family: Focusing on the occurrence, progression and treatment of cancer.Medical oncology (Northwood, London, England) · 2026Review
- RBM15 in leukemogenesis: an emerging regulator at the interface of RNA biology and hematopoiesis.Trends in cancer · 2026Review
- Methylation marks breast cancer metastasis: The roles of mThe Journal of biological chemistry · 2026Review
- RNA-binding motif proteins as context-dependent regulators of tumor-immune crosstalk, genome stability, and therapeutic vulnerabilities in cancer.Frontiers in immunology · 2026Review
- mFrontiers in cell and developmental biology · 2026Review
- The mechanism of Vicenin-2 in ameliorating skin photoaging: involvement of m6A-modified macrophage polarization.Frontiers in pharmacology · 2026Article
- Article
- Roles of tumor-associated macrophages in triple-negative breast cancer progression.Frontiers in immunology · 2025Review
- RBM15-mediated mFrontiers in cell and developmental biology · 2025Review
- m6A RNA modification in tumor-associated macrophages: emerging roles in cancer immunity.Frontiers in immunology · 2025Review
Corrections and comments
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Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundTriple-negative breast cancer (TNBC) is one of the breast cancer subtypes with a poor prognosis, and the current main treatment modalities include surgical resection and adjuvant chemotherapy. However, the development of drug resistance in tumor cells to chemotherapeutic agents poses great challenges to anticancer treatment.
methodsBioinformatics analysis was used to screen the up-regulated genes in paclitaxel (PTX)-resistant TNBC cells. Cell viability was measured by a CCK-8 kit. TNFSF9 (Tumor necrosis factor receptor superfamily member 9) protein level was detected by Western blot (WB) assay. PTX-resistant TNBC cell lines (MDA-MB-231/PTX, MDA-MB-468/PTX) were constructed and their drug resistance was shown by IC50. The EdU, flow cytometry, Transwell, and other commercial kits were applied to detect the proliferation, apoptosis, migration, invasion, macrophage M2 polarization, and glycolysis of PTX-resistant TNBC cells. RBM15 (RNA binding motif protein 15) levels were measured by RT-qPCR and WB assays. The RIP, MeRIP, and actinomycin D assays were used to analyze the interaction between TNFSF9 and RBM15. The effect of RBM15/TNFSF9 on PTX sensitivity in vivo was verified by xenograft tumor experiments.
resultsTNFSF9 was highly expressed in PTX-resistant TNBC cells. Silencing of TNFSF9 enhanced the sensitivity to PTX. Silencing TNFSF9 induced polarization of macrophages from M2 to M1 phenotype and the release of IL-1β and TNF-α, but decreased the levels of IL-10 and TGF-β. RBM15 targeted the N6-adenylate methylation (m
conclusionThis study demonstrated that RBM15 enhanced PTX resistance in TNBC by promoting m
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