ArticleScientific reports2019
ELK3 expressed in lymphatic endothelial cells promotes breast cancer progression and metastasis through exosomal miRNAs.
Article in Scientific reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.
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Who cites it
36 citing papers in PubMed, 62 citations in OpenAlex.
- ETS transcription factor ELK3: Molecular insights and translational horizons in cancer (Review).Oncology letters · 2026Review
- Article
- Transcription factors remodel tumor immune microenvironment by impacting multiple immune cells.Discover oncology · 2026Review
- Lymphatic Endothelial Cells and Organ-Associated Lymphangiogenesis in Tumor Microenvironment.Cells · 2025Review
- Axillary adipose tissue-derived lymphatic endothelial cells exhibit distinct transcriptomic signatures reflecting lymphatic invasion status in breast cancer.Breast cancer research : BCR · 2025Article
- Role of Triple-Negative Breast Cancer-Derived Extracellular Vesicles in Metastasis: Implications for Therapeutics and Biomarker Development.Journal of cellular and molecular medicine · 2025Review
- Aged breast matrix bound vesicles promote breast cancer invasiveness.Biomaterials · 2024Article
- Single-cell analysis reveals ADGRL4+ renal tubule cells as a highly aggressive cell type in clear cell renal cell carcinoma.Scientific reports · 2024Article
- Early Progression of Abdominal Aortic Aneurysm is Decelerated by Improved Endothelial Barrier Function via ALDH2-LIN28B-ELK3 Signaling.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2023Article
- The role of non-coding RNAs in extracellular vesicles in breast cancer and their diagnostic implications.Oncogene · 2023Review
- Establishment and validation of an immune infiltration predictive model for ovarian cancer.BMC medical genomics · 2023Article
- Glioma angiogenesis is boosted by ELK3 activating the HIF-1BMC cancer · 2023Article
- An IGFBP7hi endothelial cell subset drives T cell extravasation in psoriasis via endothelial glycocalyx degradation.The Journal of clinical investigation · 2023Article
- Article
- ELK3-CXCL16 axis determines natural killer cell cytotoxicity via the chemotactic activity of CXCL16 in triple negative breast cancer.Oncoimmunology · 2023Article
- Molecular Docking and Intracellular Translocation of Extracellular Vesicles for Efficient Drug Delivery.International journal of molecular sciences · 2022Review
- Circular RNA hsa_circ_0000144 aggravates ovarian Cancer progression by regulating ELK3 via sponging miR-610.Journal of ovarian research · 2022Article
- Cell Trafficking at the Intersection of the Tumor-Immune Compartments.Annual review of biomedical engineering · 2022Review
- Review
- Tumor microenvironment pathways: Cross regulation in breast cancer metastasis.Genes & diseases · 2022Review
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Tumor-associated lymphatic vessels (LV) serve as a route of cancer dissemination through the prometastatic crosstalk between lymphatic endothelial cells (LECs) lining the LVs and cancer cells. Compared to blood endothelial cell-derived angiocrine factors, however, LEC-secreted factors in the tumor microenvironment and their roles in tumor metastasis are poorly understood. Here, we report that ELK3 expressed in LECs contributes to the dissemination of cancer cells during tumor growth by providing oncogenic miRNAs to tumor cells through exosomes. We found that conditioned medium from ELK3-suppressed LECs (LCM) lost its ability to promote the migration and invasion of breast cancer cells such as MDA-MB-231, Hs578T and BT20 in vitro. Suppression of ELK3 in LECs diminished the ability of LECs to promote tumor growth and metastasis of MDA-MB-231 in vivo. Exosomes derived from LECs significantly increased the migration and invasion of MDA-MB-231 in vitro, but ELK3 suppression significantly diminished the pro-oncogenic activity of exosomes from LECs. Based on the miRNA expression profiles of LECs and functional analysis, we identified miR-503-3p, miR-4269 and miR-30e-3p as downstream targets of ELK3 in LECs, which cause the above phenotype of cancer cells. These findings strongly suggest that ELK3 expressed in LECs is a major regulator that controls the communication between the tumor microenvironment and tumors to support cancer metastasis.
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