ArticleJournal of advanced research2026
A novel peptide MIB1-223aa encoded by exosomal circMIB1 from cancer-associated fibroblasts drives triple-negative breast cancer metastasis and stemness via stabilizing MIB1 to activate Notch signaling.
Article in Journal of advanced research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers, 1 of them a synthesis that pooled it.
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Who cites it
10 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Exosomes and Triple-Negative Breast Cancer: Current Knowledge and Clinical Significance.International journal of molecular sciences · 2026Pooled it
- Exosomal circular RNAs in the tumor immune microenvironment: From regulatory mechanisms to therapeutic opportunities and translational hurdles (Review).International journal of molecular medicine · 2026Review
- Cancer-Associated Fibroblasts Promote Glucose Metabolic Reprogramming and Progression of Triple-Negative Breast Cancer via Exosomal circFAD104-Mediated Intercellular Communication.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- CAF-derived exosomes inhibit ferroptosis via GALNT14-mediated O-GalNAcylation of SLC7A11 in colorectal cancer.Oncogene · 2026Article
- Decoding the functional network of circular RNAs encoding proteins in hepatocellular carcinoma: from carcinogenesis to clinical transformation.Journal of advanced research · 2026Review
- Notch signaling in the tumor microenvironment: recent advances and targeted therapeutics.Molecular cancer · 2026Review
- Exosomes as Pivotal Mediators of Tumor-Immune Communication: Implications for Immunotherapy and Liquid Biopsy.International journal of nanomedicine · 2026Review
- Circular RNAs in cancer immunology: Immune escape, therapeutic resistance, and nanomedicine synergies.Translational oncology · 2026Article
- Functions and mechanisms of circular RNAs in cancer stem cells and therapy resistance.Frontiers in cell and developmental biology · 2026Review
- Exosome-derived Menin from cancer-associated fibroblasts promotes gastric cancer progression by activating the HSPA6/JNK/JunD pathway and inducing EMT.Journal of translational medicine · 2025Article
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15 authors.
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Abstract
introductionEmerging evidence has indicated that the complex interactions between tumor microenvironment (TME) and cancer cells play a pivotal role in driving tumor initiation and metastasis. Cancer associated fibroblasts (CAFs), major cell components in the TME, exert significant effects on malignant behaviors of various cancers. Triple negative breast cancer (TNBC) is the most malignant subtype of breast cancer with a high metastatic potential and poorer prognosis. However, the underlying mechanism by which CAFs promote TNBC development has not been sufficiently studied.
objectivesThe study aims to elucidate how CAFs promote TNBC aggressiveness by delivering protein-coding circMIB1 to activate MIB1/DLL4/Notch pathway, and provide a potential clinical biomarker for TNBC management.
methodsThe oncogenic exosomal circMIB1 with protein-coding potential was identified through high-throughput RNA sequencing and ribosome nascent-chain complex sequencing (RNC-seq). The enrichment of circMIB1 in CAFs was confirmed using in situ hybridization (ISH) and qRT-PCR. The protein-coding capacity of circMIB1 was validated based on the polysome profiling, and luciferase assays. Functional roles of circMIB1 were explored using in vitro and in vivo models, while the underlying mechanism was dissected via co-immunoprecipitation (Co-IP) and western blotting.
resultsCAF-secreted exosomal circMIB1 promoted TNBC metastasis and stemness by translating a functional peptide, MIB1-223aa. Mechanistically, MIB1-223aa competitively bound to the E3 ubiquitin ligase RNF213, which blocked the RNF213-mediated K48-linked ubiquitination and degradation of MIB1. Moreover, the stabilized MIB1 enhanced the Notch signaling via a ubiquitination-dependent activation of the ligand DLL4, thereby driving TNBC malignancy. Clinically, high expression of circMIB1 or MIB1-223aa in TNBC tissues was correlated with poor clinical prognosis, as evidenced by reduced overall survival, shortened disease-free survival, and elevated lymphatic metastasis rates.
conclusionThis study provides the first evidence of exosome-transmitted protein-coding circRNAs in CAF-TNBC crosstalk, offering novel insights into the TME-driven metastasis and providing promising biomarker for TNBC management.
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