ArticleAnti-cancer drugs2019
Downregulation of miR-205 contributes to epithelial-mesenchymal transition and invasion in triple-negative breast cancer by targeting HMGB1-RAGE signaling pathway.
Article in Anti-cancer drugs, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers, 1 of them a synthesis that pooled it.
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Who cites it
35 citing papers in PubMed, 1 synthesis or guideline pooled it, 50 citations in OpenAlex.
- Focal Adhesion Kinase (FAK)-Hippo/YAP transduction signaling mediates the stimulatory effects exerted by S100A8/A9-RAGE system in triple-negative breast cancer (TNBC).Journal of experimental & clinical cancer research : CR · 2022Pooled it
- Bioinformatics Analysis of microRNAs Associated with Metastatic Potential in Breast Cancer.Biology · 2026Article
- Targeting Triple-Negative Breast Cancer: Resistance Mechanisms and Therapeutic Advancements.Cancer medicine · 2025Review
- Decoding the Epigenome of Breast Cancer.International journal of molecular sciences · 2025Review
- The modulation of immune cell death in connection to microRNAs and natural products.Frontiers in immunology · 2024Review
- RAGE and its ligands in breast cancer progression and metastasis.Oncology reviews · 2024Review
- Impact of three miRNA signature as potential diagnostic marker for triple negative breast cancer patients.Scientific reports · 2023Article
- Exosomal miR-205-5p Improves Endometrial Receptivity by Upregulating E-Cadherin Expression through ZEB1 Inhibition.International journal of molecular sciences · 2023Article
- Adverse Crosstalk between Extracellular Matrix Remodeling and Ferroptosis in Basal Breast Cancer.Cells · 2023Article
- ER Negative Breast Cancer and miRNA: There Is More to Decipher Than What the Pathologist Can See!Biomedicines · 2023Review
- Implications of receptor for advanced glycation end products for progression from obesity to diabetes and from diabetes to cancer.World journal of diabetes · 2023Review
- Insulin/IGF Axis and the Receptor for Advanced Glycation End Products: Role in Meta-inflammation and Potential in Cancer Therapy.Endocrine reviews · 2023Review
- Co-Expression of Podoplanin and CD44 in Proliferative Vitreoretinopathy Epiretinal Membranes.International journal of molecular sciences · 2023Review
- The Role of miRNAs in the Prognosis of Triple-Negative Breast Cancer: A Systematic Review and Meta-Analysis.Diagnostics (Basel, Switzerland) · 2022Review
- Upregulated GATA3/miR205-5p Axis Inhibits MFNG Transcription and Reduces the Malignancy of Triple-Negative Breast Cancer.Cancers · 2022Article
- HMGB1 mediates invasion and PD-L1 expression through RAGE-PI3K/AKT signaling pathway in MDA-MB-231 breast cancer cells.BMC cancer · 2022Article
- Targeting HMGB1: An available Therapeutic Strategy for Breast Cancer Therapy.International journal of biological sciences · 2022Review
- Current and Future Therapies for Immunogenic Cell Death and Related Molecules to Potentially Cure Primary Breast Cancer.Cancers · 2021Review
- Tumor Microenvironment: Key Players in Triple Negative Breast Cancer Immunomodulation.Cancers · 2021Review
- Damage-Associated Molecular Patterns Modulation by microRNA: Relevance on Immunogenic Cell Death and Cancer Treatment Outcome.Cancers · 2021Review
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Our aim was to study the regulatory molecule networks involved in the epithelial-to-mesenchymal transition and thus promoting the early onset of metastasis in triple-negative breast cancer (TNBC). Forty pairs of human TNBC and their adjacent normal breast tissues were analyzed by real-time PCR and immunochemistry to demonstrate the correlation between the miR-205 expression and clinicopathological characteristics. In vitro, 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2-H-tetrazolium bromide assay, cell migration, and invasion assay were used to detect the cell growth and invasive ability of TNBC cells after upregulation or downregulation of miR-205 expression. Luciferase reporter assay was used to confirm the potential target directly influenced by miR-205. Our results showed that miR-205 abnormal expression may be involved and associated with the biological traits of TNBC. Ectopic expression of miR-205 not only inhibited cell growth, but also suppressed migration and invasion of mesenchymal-like TNBC cells. In addition, we found that overexpression of miR-205 significantly suppressed HMGB1 by binding its 3'-untranslated region, and that miR-205 was inversely correlated with the expression of HMGB1 and RAGE in cell lines and clinical samples. Our study illustrated that miR-205 was a tumor suppressor in TNBC, which attenuated the viability and the acquisition of the epithelial-to-mesenchymal transition phenotype TNBC cells at least partially exerted through targeting of HMGB1-RAGE signaling pathway.
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