ArticleCarcinogenesis2015
miR-200a inhibits migration of triple-negative breast cancer cells through direct repression of the EPHA2 oncogene.
Article in Carcinogenesis, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers.
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Who cites it
51 citing papers in PubMed, 106 citations in OpenAlex.
- Integrative analysis of TCGA data identifies hsa-miR-200a as a breast cancer-associated microRNA biomarker with exploratory serum validation.Genes & genomics · 2026Article
- Role and underlying mechanisms of miR‑200 family in breast cancer (Review).International journal of oncology · 2026Review
- Extracellular vesicles and miRNA-based therapies in triple-negative breast cancer: advances and clinical perspectives.Extracellular vesicles and circulating nucleic acids · 2025Review
- Evaluation of tumorigenesis-related miRNAs in breast cancer in Egyptian women: a retrospective, exploratory analysis.Scientific reports · 2024Article
- Targeting the EphA2 pathway: could it be the way for bone sarcomas?Cell communication and signaling : CCS · 2024Review
- The TGFβ2-Snail1-miRNAClinical and translational medicine · 2024Article
- Targeted therapy approaches for epithelial-mesenchymal transition in triple negative breast cancer.Frontiers in oncology · 2024Review
- Eph receptors and ephrins in cancer progression.Nature reviews. Cancer · 2024Review
- New Biomarkers and Treatment Advances in Triple-Negative Breast Cancer.Diagnostics (Basel, Switzerland) · 2023Review
- Review
- Targeting the KLF5-EphA2 axis can restrain cancer stemness and overcome chemoresistance in basal-like breast cancer.International journal of biological sciences · 2023Article
- The functional significance and cross-talk of non-coding RNAs in triple negative and quadruple negative breast cancer.Molecular biology reports · 2022Review
- The role of miR-200 family in the regulation of hallmarks of cancer.Frontiers in oncology · 2022Review
- Expression Profiles of Estrogen-Regulated MicroRNAs in Cancer Cells.Methods in molecular biology (Clifton, N.J.) · 2022Article
- Combined analysis of miR-200 family and its significance for breast cancer.Scientific reports · 2021Article
- HOXA1 Is an Antagonist of ERα in Breast Cancer.Frontiers in oncology · 2021Article
- Aberrant Expressional Profiling of Small RNA by Cold Atmospheric Plasma Treatment in Human Chronic Myeloid Leukemia Cells.Frontiers in genetics · 2021Article
- Discovery and Pharmacological Evaluation of STEAP4 as a Novel Target for HER2 Overexpressing Breast Cancer.Frontiers in oncology · 2021Article
- Modulatory Role of microRNAs in Triple Negative Breast Cancer with Basal-Like Phenotype.Cancers · 2020Review
- The EphA2 and cancer connection: potential for immune-based interventions.Molecular biology reports · 2020Review
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 3 countries.
Funding
Abstract
Triple-negative breast cancer (TNBC) is characterized by aggressiveness and affects 10-20% of breast cancer patients. Since TNBC lacks expression of ERα, PR and HER2, existing targeted treatments are not effective and the survival is poor. In this study, we demonstrate that the tumor suppressor microRNA miR-200a directly regulates the oncogene EPH receptor A2 (EPHA2) and modulates TNBC migration. We show that EPHA2 expression is correlated with poor survival specifically in basal-like breast cancer and that its expression is repressed by miR-200a through direct interaction with the 3'UTR of EPHA2. This regulation subsequently affects the downstream activation of AMP-activated protein kinase (AMPK) and results in decreased cell migration of TNBC. We establish that miR-200a directs cell migration in a dual manner; in addition to regulating the well-characterized E-cadherin pathway it also regulates a EPHA2 pathway. The miR-200a-EPHA2 axis is a novel mechanism highlighting the possibility of utilizing miR-200a delivery to target TNBC metastases.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.