ArticleMolecular oncology2014
miR-206 inhibits cell migration through direct targeting of the actin-binding protein coronin 1C in triple-negative breast cancer.
Article in Molecular oncology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers.
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Who cites it
57 citing papers in PubMed, 115 citations in OpenAlex.
- Circulating MicroRNA in Breast Cancer.Cancers · 2026Review
- The Role of Actin-Binding Proteins in Breast Cancer Progression.Breast cancer (Dove Medical Press) · 2026Review
- The Role of Non-Coding Regions in Breast Cancer: From Gene Regulation to Therapeutic Implications.Pharmaceuticals (Basel, Switzerland) · 2025Review
- CORO1C Regulates the Malignant Biological Behavior of Ovarian Cancer Cells and Modulates the mRNA Expression Profile through the PI3K/AKT Signaling Pathway.Cell biochemistry and biophysics · 2025Article
- DIFFERENTIALLY EXPRESSED MIRNAS EXPLAIN RACIAL DIFFERENCES IN DIAGNOSIS STAGE AMONG TRIPLE NEGATIVE BREAST CANCER PATIENTS IN LOUISIANA.jLPHA : the official journal of the Louisiana Public Health Association · 2025Article
- Circular RNA circ-SLC7A5 Functions as a Competing Endogenous RNA to Impact Cell Biological Behaviors in Esophageal Squamous Cell Carcinoma (ESCC).Cell biochemistry and biophysics · 2024Article
- New Biomarkers and Treatment Advances in Triple-Negative Breast Cancer.Diagnostics (Basel, Switzerland) · 2023Review
- Propofol mediates non-small cell lung cancer growth in part by regulating circ_0003028-related mechanisms.Thoracic cancer · 2023Article
- Article
- Emerging roles and mechanisms of miR-206 in human disorders: a comprehensive review.Cancer cell international · 2022Review
- The functional significance and cross-talk of non-coding RNAs in triple negative and quadruple negative breast cancer.Molecular biology reports · 2022Review
- CORO1C, a novel PAK4 binding protein, recruits phospho-PAK4 at serine 99 to the leading edge and promotes the migration of gastric cancer cells.Acta biochimica et biophysica Sinica · 2022Article
- Exploring the Immune Infiltration Landscape and M2 Macrophage-Related Biomarkers of Proliferative Diabetic Retinopathy.Frontiers in endocrinology · 2022Article
- Molecular Pathogenesis of the Coronin Family:International journal of molecular sciences · 2021Article
- The Role of WAVE2 Signaling in Cancer.Biomedicines · 2021Review
- Autophagy-related circRNA evaluation reveals hsa_circ_0001747 as a potential favorable prognostic factor for biochemical recurrence in patients with prostate cancer.Cell death & disease · 2021Article
- Improved delivery of miR-1296 loaded cationic nanoliposomes for effective suppression of triple negative breast cancer.Saudi pharmaceutical journal : SPJ : the official publication of the Saudi Pharmaceutical Society · 2021Article
- The Anticancer Effects of Flavonoids through miRNAs Modulations in Triple-Negative Breast Cancer.Nutrients · 2021Review
- Article
- Construction and Comparison of ceRNA Regulatory Network for Different Age Female Breast Cancer.Frontiers in genetics · 2021Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Patients with triple-negative breast cancer (TNBC) have an overall poor prognosis, which is primarily due to a high metastatic capacity of these tumors. Novel therapeutic approaches to target the signaling pathways that promote metastasis are desirable, in order to improve the outcome for these patients. A loss of function of a microRNA, miR-206, is related to increased metastasis potential in breast cancers but the mechanism is not known. In this study, we show that miR-206 was decreased in TNBC clinical tumor samples and cell lines whereas one of its predicted targets, actin-binding protein CORO1C, was increased. Expression of miR-206 significantly reduced proliferation and migration while repressing CORO1C mRNA and protein levels. We demonstrate that miR-206 interacts with the 3'-untranslated region (3'-UTR) of CORO1C and regulates this gene post-transcriptionally. This post-transcriptional regulation was dependent on two miR-206-binding sites within the 3'-UTR of CORO1C and was relieved by mutations of corresponding sites. Further, silencing of CORO1C reduced tumor cell migration and affected the actin skeleton and cell morphology, similar to miR-206 expression, but did not reduce proliferation. In accordance with this, overexpression of CORO1C rescued the inhibitory effect of miR-206 on cell migration. Our findings suggest that miR-206 represses tumor cell migration through direct targeting of CORO1C in TNBC cells which modulates the actin filaments. This pathway is a novel mechanism that offers a mechanistic basis through which the metastatic potential of TNBC tumors could be targeted.
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