Related Experiment Video
Updated: May 28, 2025

An Enrichment Method for Small Extracellular Vesicles Derived from Liver Cancer Tissue
Published on: February 3, 2023
BANCR-containing extracellular vesicles enhance breast cancer resistance
Xinming Song1, Shen Liu1, Ying Zeng1
1Department of Head and Neck Oncology, Affiliated Hospital of Guangdong Medical University, Zhanjiang, China.
Abstract:
Extracellular vesicles (EVs) are nano-sized particles secreted by many cell types-including tumor cells-and play key roles in cellular communication by transporting functional RNAs. This study aims to elucidate the role of long noncoding RNA BRAF-activated nonprotein coding RNA (BANCR) in EVs derived from breast cancer (BC) cells in trastuzumab resistance. Differentially expressed long noncoding RNA and downstream targets in BC-resistant samples were identified. SKBR-3 cells were treated with trastuzumab to generate resistant cells (SKBR-3TR), and EVs from these cells (SKBR-3TR-EVs) were isolated and characterized. Functional studies of BANCR were performed in SKBR-3 and SKBR-3TR cells. Coculturing SKBR-3 cells with SKBR-3TR-EVs assessed changes in cell behavior. A xenograft model in nude mice examined in vivo tumorigenicity and trastuzumab resistance. BANCR was highly expressed in SKBR-3TR cells and EVs, linked to trastuzumab resistance. SKBR-3TR-EVs transferred BANCR to SKBR-3 cells, where BANCR inhibited miR-34a-5p, reducing its expression. High-mobility group A1 (HMGA1) was identified as a miR-34a-5p target. BANCR activated the HMGA1/Wnt/β-catenin pathway by inhibiting miR-34a-5p, promoting resistance. In vivo experiments showed that BANCR inhibition delayed tumorigenesis and reversed trastuzumab resistance. BC cell-derived EVs containing BANCR may enhance resistance to trastuzumab by regulating the miR-34a-5p/HMGA1/Wnt/β-catenin axis, presenting a potential target for BC therapy.
Related Concept Videos
Receptor Downregulation in MVBs
The EGFR can initiate signaling pathways that lead to cell proliferation, migration, and differentiation. Overexpression of EGFR stimulates cells to proliferate. Excessive EGFR...
Cancer Stem Cells and Tumor Maintenance
Cancer stem cells are thought to originate from tissue-specific normal stem cells or progenitor cells. The normal stem cells usually reside in...
Metastasis
Epithelial-to-Mesenchymal Transition
The epithelial-to-mesenchymal transition or EMT is a developmental process commonly observed in wound healing, embryogenesis, and cancer metastasis. EMT is induced by transforming growth factor-beta (TGF-β) or receptor tyrosine kinase (RTK) ligands, which further...
Overview of Exosomes
Stahl et al. discovered exosomes in 1983, but the exosomes were initially considered waste products released from the...
The Tumor Microenvironment
Intralumenal Vesicles and Multivesicular Bodies

