ArticleCell cycle (Georgetown, Tex.)2014
miR-221/222 control luminal breast cancer tumor progression by regulating different targets.
Article in Cell cycle (Georgetown, Tex.), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 47 citations in OpenAlex.
- Regulation of Different Types of Cell Death by Noncoding RNAs: Molecular Insights and Therapeutic Implications.ACS pharmacology & translational science · 2025Review
- Non-coding RNAs, a double-edged sword in breast cancer prognosis.Cancer cell international · 2025Review
- Non-coding RNAs: Emerging contributors to chemoresistance in chronic myeloid leukemia.Leukemia research reports · 2025Review
- Notch3 restricts metastasis of breast cancers through regulation of the JAK/STAT5A signaling pathway.BMC cancer · 2023Article
- Hsa-miR-221-3p promotes proliferation and migration in HER2-positive breast cancer cells by targeting LASS2 and MBD2.Histology and histopathology · 2022Article
- Non-Coding RNAs Are Implicit in Chronic Myeloid Leukemia Therapy Resistance.International journal of molecular sciences · 2022Review
- miR-221/222 as biomarkers and targets for therapeutic intervention on cancer and other diseases: A systematic review.Molecular therapy. Nucleic acids · 2022Review
- microRNA-221 and tamoxifen resistance in luminal-subtype breast cancer patients: A case-control study.Annals of medicine and surgery (2012) · 2022Article
- Microarray meta-analysis reveals IL6 and p38β/MAPK11 as potential targets of hsa-miR-124 in endothelial progenitor cells: Implications for stent re-endothelization in diabetic patients.Frontiers in cardiovascular medicine · 2022Article
- Noncoding RNAs in tumor metastasis: molecular and clinical perspectives.Cellular and molecular life sciences : CMLS · 2021Review
- MicroRNA-221 regulates cell activity and apoptosis in acute lymphoblastic leukemia via regulating PTEN.Experimental and therapeutic medicine · 2021Article
- MicroRNAs: The Link between the Metabolic Syndrome and Oncogenesis.International journal of molecular sciences · 2021Review
- Review
- Identification of microRNA clusters cooperatively acting on epithelial to mesenchymal transition in triple negative breast cancer.Nucleic acids research · 2019Article
- Long non-coding RNA p10247, high expressed in breast cancer (lncRNA-BCHE), is correlated with metastasis.Clinical & experimental metastasis · 2018Article
- Changes in miR-221/222 Levels in Invasive and In Situ Carcinomas of the Breast: Differences in Association with Estrogen Receptor and TIMP3 Expression Levels.Molecular diagnosis & therapy · 2016Article
- New Concepts in Cancer Biomarkers: Circulating miRNAs in Liquid Biopsies.International journal of molecular sciences · 2016Review
- Article
- miR-221 facilitates the TGFbeta1-induced epithelial-mesenchymal transition in human bladder cancer cells by targeting STMN1.BMC urology · 2015Article
Corrections and comments
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Authors and funding
13 authors at 6 institutions in 4 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
α6β4 integrin is an adhesion molecule for laminin receptors involved in tumor progression. We present a link between β4 integrin expression and miR-221/222 in the most prevalent human mammary tumor: luminal invasive carcinomas (Lum-ICs). Using human primary tumors that display different β4 integrin expression and grade, we show that miR-221/222 expression inversely correlates with tumor proliferating index, Ki67. Interestingly, most high-grade tumors express β4 integrin and low miR-221/222 levels. We ectopically transfected miR-221/222 into a human-derived mammary tumor cell line that recapitulates the luminal subtype to investigate whether miR-221/222 regulates β4 expression. We demonstrate that miR-221/222 overexpression results in β4 expression downregulation, breast cancer cell proliferation, and invasion inhibition. The role of miR-221/222 in driving β4 integrin expression is also confirmed via mutating the miR-221/222 seed sequence for β4 integrin 3'UTR. Furthermore, we show that these 2 miRNAs are also key breast cancer cell proliferation and invasion regulators, via the post-transcriptional regulation of signal transducer and activator of transcription 5A (STAT5A) and of a disintegrin and metalloprotease-17 (ADAM-17). We further confirm these data by silencing ADAM-17, using a dominant-negative or an activated STAT5A form. miR-221/222-driven β4 integrin, STAT5A, and ADAM-17 did not occur in MCF-10A cells, denoted "normal" breast epithelial cells, indicating that the mechanism is cancer cell-specific. These results provide the first evidence of a post-transcriptional mechanism that regulates β4 integrin, STAT5A, and ADAM-17 expression, thus controlling breast cancer cell proliferation and invasion. Pre-miR-221/222 use in the aggressive luminal subtype may be a powerful therapeutic anti-cancer strategy.
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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.