ArticleBreast cancer (Tokyo, Japan)2023
Breast cancer-derived exosomal lncRNA SNHG14 induces normal fibroblast activation to cancer-associated fibroblasts via the EBF1/FAM171A1 axis.
Article in Breast cancer (Tokyo, Japan), 2023. 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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Who cites it
10 citing papers in PubMed, 13 citations in OpenAlex.
- Whole-transcriptome sequencing reveals hypoxic esophageal squamous cell carcinoma-derived migrasomes driving cancer-associated fibroblast activation.Briefings in functional genomics · 2026Article
- EBF1 Deficiency Drives Prostate Cancer Progression by Interfering with the Transcriptional Regulation ofOncology research · 2026Article
- CAF-derived exosomes: orchestrators of dysregulated signaling pathways in breast cancer progression.Naunyn-Schmiedeberg's archives of pharmacology · 2026Review
- Advances in Research on the B-Lineage Transcription Factor EBF1 in Solid Tumors.International journal of molecular sciences · 2025Review
- Exosome-Mediated Cellular Communication in the Tumor Microenvironment Imparts Drug Resistance in Breast Cancer.Cancers · 2025Review
- Investigating the role of exosomal long non-coding RNAs in drug resistance within female reproductive system cancers.Frontiers in cell and developmental biology · 2025Review
- The role of ceRNAs in breast cancer microenvironmental regulation and therapeutic implications.Journal of molecular medicine (Berlin, Germany) · 2025Review
- Snhg14/miR-181a-5p axis-mediated "M1" macrophages aggravate LPS-induced myocardial cell injury.Heliyon · 2024Article
- Identification of hub lncRNAs correlated with tetralogy of fallot based on weighted gene co-expression network analysis.Biochemistry and biophysics reports · 2024Article
- Review
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundExosomes released from cancer cells can activate normal fibroblasts (NFs) into cancer-associated fibroblasts (CAFs), which promotes cancer development. Our study aims to explore the role and potential mechanisms of breast cancer exosomes-delivered long non-coding RNA (lncRNA) SNHG14 in regulating CAFs transformation.
methodsAdjacent normal tissues, cancerous and serum specimens were gathered in breast cancer patients. Exosomes and NFs were separated from breast cancer cells (SKBR-3) and normal tissues of patients, respectively. Cell viability and migration were measured with CCK-8 and Transwell assays. CAFs markers, fibroblast activation protein (FAP) and a-smooth muscle actin (α-SMA) were detected for assessing CAFs activation. The interactions between molecules were evaluated using dual luciferase reporter assay, RNA immunoprecipitation and chromatin immunoprecipitation.
resultsSNHG14 and FAM171A1 were upregulated in breast cancer. Exosomes secreted by SKBR-3 cells induced NFs activation in CAFs, as indicated by upregulating CAFs marker levels and facilitated cell viability and migration. Exosomal SNHG14 silencing in SKBR-3 cells inhibited CAFs activation. SNHG14 positively regulated FAM171A1 expression through EBF1. FAM171A1 overexpression eliminated the inhibition effect of exosomal SNHG14 silencing in CAFs transformation.
conclusionBreast cancer-derived exosomal SNHG14 contributed to NFs transformation into CAFs by the EBF1/FAM171A1 axis.
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