ArticleScientific reports2016
Genome-wide identification of target genes for miR-204 and miR-211 identifies their proliferation stimulatory role in breast cancer cells.
Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers, 1 of them a synthesis that pooled it.
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Who cites it
24 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Expression and potential molecular mechanisms of miR‑204‑5p in breast cancer, based on bioinformatics and a meta‑analysis of 2,306 cases.Molecular medicine reports · 2019Pooled it
- Evolution in metazoans of the TRPM channel family involves multiple gains and losses of genes and domains.Molecular biology and evolution · 2026Article
- The Multifaceted Role of miR-211 in Health and Disease.Biomolecules · 2025Review
- Review
- Disturbed flow regulates protein disulfide isomerase A1 expression via microRNA-204.Frontiers in physiology · 2024Article
- The role of TXNIP in cancer: a fine balance between redox, metabolic, and immunological tumor control.British journal of cancer · 2023Review
- Identification of cuproptosis-related gene SLC31A1 and upstream LncRNA-miRNA regulatory axis in breast cancer.Scientific reports · 2023Article
- Article
- Thioredoxin-Interacting Protein in Cancer and Diabetes.Antioxidants & redox signaling · 2022Review
- The Paradoxical Behavior of microRNA-211 in Melanomas and Other Human Cancers.Frontiers in oncology · 2020Review
- Upregulation of miR-211 Promotes Chondrosarcoma Development via Targeting Tumor Suppressor VHL.OncoTargets and therapy · 2020Article
- Regulation of phagolysosomal activity by miR-204 critically influences structure and function of retinal pigment epithelium/retina.Human molecular genetics · 2019Article
- Article
- Identification of competitive endogenous RNAs network in breast cancer.Cancer medicine · 2019Article
- microRNA-211 regulates cell proliferation, apoptosis and migration/invasion in human osteosarcoma via targeting EZRIN.Cellular & molecular biology letters · 2019Article
- Ginsenoside Rh2 epigenetically regulates cell-mediated immune pathway to inhibit proliferation of MCF-7 breast cancer cells.Journal of ginseng research · 2018Article
- miR-204-5p and miR-3065-5p exert antitumor effects on melanoma cells.Oncology letters · 2018Article
- MicroRNA-211 suppresses prostate cancer proliferation by targeting SPARC.Oncology letters · 2018Article
- miR-204-5p and miR-211-5p Contribute to BRAF Inhibitor Resistance in Melanoma.Cancer research · 2018Article
- miR-204-5p suppresses hepatocellular cancer proliferation by regulating homeoprotein SIX1 expression.FEBS open bio · 2018Article
Corrections and comments
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Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
MiR-204 and miR-211 (miR-204/211) share the same seed site sequence, targeting many of the same genes. Their role in cancer development remains controversial, as both cell proliferative and suppressive effects have been identified. This study aimed to address the relationship between the two structurally similar microRNAs (miRs) by examining their target genes in depth as well as to reveal their contribution in breast cancer cells. Genome-wide pathway analysis with the dysregulated genes after overexpression of either of the two miRs in MCF-7 breast cancer cell identified the "Cancer"- and "Cell signaling"-related pathway as the top pathway for miR-204 and miR-211, respectively. The majority of the target genes for both miRs notably comprised ones that have been characterized to drive cells anti-tumorigenic. Accordingly, the miRs induced the proliferation of MCF-7 and MDA-MB-231 cells, judged by cell proliferation as well as colony forming assay. Tumor suppressors, MX1 and TXNIP, were proven to be direct targets of the miRs. In addition, a high association was observed between miR-204 and miR-211 expression in breast cancer tissue. Our results indicate that miR-204/211 serve to increase cell proliferation at least in MCF-7 and MDA-MB-231 breast cancer cells by downregulating tumor suppressor genes.
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