ArticleOncogene2014
Loss of the polycomb protein Mel-18 enhances the epithelial-mesenchymal transition by ZEB1 and ZEB2 expression through the downregulation of miR-205 in breast cancer.
Article in Oncogene, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 72 papers.
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Who cites it
72 citing papers in PubMed, 111 citations in OpenAlex.
- miR‑205: A dual regulator of angiogenesis in health and disease (Review).International journal of molecular medicine · 2026Review
- Recent progress in immune evasion mechanisms of triple-negative breast cancer.Journal of translational medicine · 2025Review
- Role of EMT in drug resistance of breast cancer: molecular mechanisms and therapeutic strategies.Frontiers in oncology · 2025Review
- Micro-RNAs in breast cancer progression and metastasis: A chromatin and metabolic perspective.Heliyon · 2024Review
- microRNA-205 represses breast cancer metastasis by perturbing the rab coupling protein [RCP]-mediated integrin β1 recycling on the membrane.Apoptosis : an international journal on programmed cell death · 2024Article
- miR-205-5p inhibits homocysteine-induced pulmonary microvascular endothelium dysfunction by targeting FOXO1.Acta biochimica et biophysica Sinica · 2023Article
- Review
- Crosstalk between Methylation and ncRNAs in Breast Cancer: Therapeutic and Diagnostic Implications.International journal of molecular sciences · 2022Review
- Critical Roles of Polycomb Repressive Complexes in Transcription and Cancer.International journal of molecular sciences · 2022Review
- Beyond Genetics: Metastasis as an Adaptive Response in Breast Cancer.International journal of molecular sciences · 2022Review
- Mechanisms of Polycomb group protein function in cancer.Cell research · 2022Review
- Induction of Paraptotic Cell Death in Breast Cancer Cells by a Novel Pyrazolo[3,4-Antioxidants (Basel, Switzerland) · 2022Article
- miR-205-5p Downregulation andInternational journal of molecular sciences · 2021Article
- Towards Unravelling the Role of ERα-Targeting miRNAs in the Exosome-Mediated Transferring of the Hormone Resistance.Molecules (Basel, Switzerland) · 2021Article
- LW1497, an Inhibitor of Malate Dehydrogenase, Suppresses TGF-β1-Induced Epithelial-Mesenchymal Transition in Lung Cancer Cells by Downregulating Slug.Antioxidants (Basel, Switzerland) · 2021Article
- Influence of chronic inflammation on the malignant phenotypes and the plasticity of colorectal cancer cells.Biochemistry and biophysics reports · 2021Article
- Review
- Interplay between p53 and non-coding RNAs in the regulation of EMT in breast cancer.Cell death & disease · 2021Review
- Targeting ferroptosis for cancer therapy: iron metabolism and anticancer immunity.American journal of cancer research · 2021Article
- miR-205 in Breast Cancer: State of the Art.International journal of molecular sciences · 2020Review
12 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The epithelial-mesenchymal transition (EMT) is the pivotal mechanism underlying the initiation of cancer invasion and metastasis. Although Mel-18 has been implicated in several biological processes in cancer, its function in the EMT of human cancers has not yet been studied. Here, we demonstrate that Mel-18 negatively regulates the EMT by epigenetically modulating miR-205. We identified miR-205 as a novel target of Mel-18 using a microRNA microarray analysis and found that Mel-18 increased miR-205 transcription by the inhibition of DNA methyltransferase-mediated DNA methylation of the miR-205 promoter, thereby downregulating its target genes, ZEB1 and ZEB2. Furthermore, the loss of Mel-18 promoted ZEB1- and ZEB2-mediated downregulation of E-cadherin transcription and also enhanced the expression of mesenchymal markers, leading to increased migration and invasion in MCF-7 cells. In MDA-MB-231 cells, Mel-18 overexpression restored E-cadherin expression, resulting in reduced migration and invasion. These effects were reversed by miR-205 overexpression or inhibition. A tumor xenograft with Mel-18 knockdown MCF-7 cells consistently showed increased ZEB1 and ZEB2 expression and decreased E-cadherin expression. Taken together, these results suggest that Mel-18 functions as a tumor suppressor by its novel negative control of the EMT, achieved through regulating the expression of miR-205 and its target genes, ZEB1 and ZEB2.
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