ArticleCell cycle (Georgetown, Tex.)2013
Activation of miR200 by c-Myb depends on ZEB1 expression and miR200 promoter methylation.
Article in Cell cycle (Georgetown, Tex.), 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers, 1 of them a synthesis that pooled it.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
28 citing papers in PubMed, 1 synthesis or guideline pooled it, 44 citations in OpenAlex.
- Large scale integration of drug-target information reveals poly-pharmacological drug action mechanisms in tumor cell line growth inhibition assays.Oncotarget · 2014Pooled it
- Emerging role of MYB transcription factors in cancer drug resistance.Cancer drug resistance (Alhambra, Calif.) · 2024Review
- Boolean modeling of mechanosensitive epithelial to mesenchymal transition and its reversal.iScience · 2023Article
- Global alteration of colonic microRNAome landscape associated with inflammatory bowel disease.Frontiers in immunology · 2022Article
- Intricate crosstalk between MYB and noncoding RNAs in cancer.Cancer cell international · 2021Review
- The miR-200 Family of microRNAs: Fine Tuners of Epithelial-Mesenchymal Transition and Circulating Cancer Biomarkers.Cancers · 2021Review
- Overlapping targets exist between the Par-4 and miR-200c axis which regulate EMT and proliferation of pancreatic cancer cells.Translational oncology · 2021Article
- miR-639 Expression Is Silenced by DNMT3A-Mediated Hypermethylation and Functions as a Tumor Suppressor in Liver Cancer Cells.Molecular therapy : the journal of the American Society of Gene Therapy · 2020Article
- miR-200 affects tamoxifen resistance in breast cancer cells through regulation of MYB.Scientific reports · 2019Article
- MicroRNA-141 protects PC12 cells against hypoxia/reoxygenation-induced injury via regulating Keap1-Nrf2 signaling pathway.Journal of bioenergetics and biomembranes · 2019Article
- Encapsulated miR-200c and Nkx2.1 in a nuclear/mitochondria transcriptional regulatory network of non-metastatic and metastatic lung cancer cells.BMC cancer · 2019Article
- Genome-wide binding of transcription factor ZEB1 in triple-negative breast cancer cells.Journal of cellular physiology · 2018Article
- Functional Role of Non-Coding RNAs during Epithelial-To-Mesenchymal Transition.Non-coding RNA · 2018Review
- A new method to study the change of miRNA-mRNA interactions due to environmental exposures.Bioinformatics (Oxford, England) · 2017Article
- Article
- miR-200c: a versatile watchdog in cancer progression, EMT, and drug resistance.Journal of molecular medicine (Berlin, Germany) · 2016Review
- ZNF281 contributes to the DNA damage response by controlling the expression of XRCC2 and XRCC4.Oncogene · 2016Article
- LncRNA PANDAR regulates the G1/S transition of breast cancer cells by suppressing p16(INK4A) expression.Scientific reports · 2016Article
- The miR-200 family and the miR-183~96~182 cluster target Foxf2 to inhibit invasion and metastasis in lung cancers.Oncogene · 2016Article
- A Polycomb-mir200 loop regulates clinical outcome in bladder cancer.Oncotarget · 2015Article
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 3 countries.
Funding
Abstract
Tumor progression to metastasis is a complex, sequential process that requires proliferation, resistance to apoptosis, motility and invasion to colonize at distant sites. The acquisition of these features implies a phenotypic plasticity by tumor cells that must adapt to different conditions by modulating several signaling pathways (1) during the journey to the final site of metastasis. Several transcription factors and microRNA play a role in tumor progression, but less is known about the control of their expression during this process. Here, we demonstrate by ectopic expression and gene silencing that the proto-oncogene c-Myb activates the expression of the 5 members of miR200 family (miR200b, miR200a, miR429, miR200c and miR141) that are involved in the control of epithelial-mesenchymal transition (EMT) and metastasis in many types of cancers. Transcriptional activation of miR200 by c-Myb occurs through binding to myb binding sites located in the promoter regions of miR200 genes on human chromosomes 1 and 12. Furthermore, when c-Myb and the transcriptional repressor ZEB1 are co-expressed, as at the onset EMT, the repression by ZEB1 prevails over the activation by c-Myb, and the expression of miR200 is inhibited. We also demonstrate that during EMT induced by TGF-β, the promoters of miR200 genes are methylated, and their transcription is repressed regardless of the presence of repressors such as ZEB1 and activators such as c-Myb. Finally, we find a correlation between the expression of c-Myb and that of four out of 5 miR200 in a data set of 207 breast cancer patients.
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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.