The miR-200 and miR-221/222 microRNA families: opposing effects on epithelial identity - Wikidata - awgldk - TriplyDB

The miR-200 and miR-221/222 microRNA families: opposing effects on epithelial identity

The miR-200 and miR-221/222 microRNA families: opposing effects on epithelial identity

http://www.wikidata.org/entity/Q27010233

about

MiRNAs and Other Epigenetic Changes as Biomarkers in Triple Negative Breast Cancer Roles for miRNAs in endocrine resistance in breast cancer Human miR-221/222 in Physiological and Atherosclerotic Vascular Remodeling TGF-β/Smad signaling in renal fibrosis MicroRNAs in Diabetic Kidney Disease MicroRNAs that affect prostate cancer: emphasis on prostate cancer in African Americans miR-221 promotes tumorigenesis in human triple negative breast cancer cells.Re-expression of miR-200c suppresses proliferation, colony formation and in vivo tumor growth of murine claudin-low mammary tumor cells.MicroRNA-200b suppresses arsenic-transformed cell migration by targeting protein kinase Cα and Wnt5b-protein kinase Cα positive feedback loop and inhibiting Rac1 activation MicroRNA-200b targets protein kinase Cα and suppresses triple-negative breast cancer metastasis Correlation between Slug transcription factor and miR-221 in MDA-MB-231 breast cancer cells.MicroRNA-200 family modulation in distinct breast cancer phenotypes.miR-200c targets a NF-κB up-regulated TrkB/NTF3 autocrine signaling loop to enhance anoikis sensitivity in triple negative breast cancer Integrated microRNA and mRNA signatures associated with survival in triple negative breast cancer.Circulating miR-221 expression level and prognosis of cutaneous malignant melanoma.Reduced expression of miR-200 family members contributes to antiestrogen resistance in LY2 human breast cancer cells MicroRNAs in renal fibrosis.CD95 and CD95L promote and protect cancer stem cells TWIST1-Induced miR-424 Reversibly Drives Mesenchymal Programming while Inhibiting Tumor Initiation.miRNAs and estrogen action.Identification of biological targets of therapeutic intervention for clear cell renal cell carcinoma based on bioinformatics approach The relevance of the TGF-β Paradox to EMT-MET programs MicroRNA and nephropathy: emerging concepts.MiR-221/-222 differentiate prognostic groups in advanced breast cancers and influence cell invasion.Intrinsic cellular signaling mechanisms determine the sensitivity of cancer cells to virus-induced apoptosis.A 22q11.2 amplification in the region encoding microRNA-650 correlates with the epithelial to mesenchymal transition in breast cancer primary cultures of Mexican patients.The proto-oncogene KRAS is targeted by miR-200c.MicroRNA-222-3p/GNAI2/AKT axis inhibits epithelial ovarian cancer cell growth and associates with good overall survival.miRNA profiling of cancer.miR-221/222: promising biomarkers for breast cancer.Effects of ARHI on breast cancer cell biological behavior regulated by microRNA-221.Non-coding RNAs in Mammary Gland Development and Disease.microRNAs in Diabetic Kidney Disease.Triple negative breast cancer: the kiss of death.miR-221/222 induces pancreatic cancer progression through the regulation of matrix metalloproteinases.Growth inhibitory effects of miR-221 and miR-222 in non-small cell lung cancer cells.miR-200c modulates ovarian cancer cell metastasis potential by targeting zinc finger E-box-binding homeobox 2 (ZEB2) expression.Downregulation of miR-221/222 enhances sensitivity of breast cancer cells to tamoxifen through upregulation of TIMP3.Mammalian APE1 controls miRNA processing and its interactome is linked to cancer RNA metabolism.Roles of microRNAs and RNA-Binding Proteins in the Regulation of Colorectal Cancer Stem Cells.

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The miR-200 and miR-221/222 microRNA families: opposing effects on epithelial identity

http://www.wikidata.org/entity/Q27010233

description

2012 nî lūn-bûn

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2012 թուականի Մարտին հրատարակուած գիտական յօդուած

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2012 թվականի մարտին հրատարակված գիտական հոդված

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2012年の論文

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2012年論文

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2012年論文

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2012年論文

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2012年論文

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2012年論文

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2012年论文

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name

The miR-200 and miR-221/222 microRNA families: opposing effects on epithelial identity

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The miR-200 and miR-221/222 microRNA families: opposing effects on epithelial identity

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The miR-200 and miR-221/222 microRNA families: opposing effects on epithelial identity

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type

label

The miR-200 and miR-221/222 microRNA families: opposing effects on epithelial identity

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The miR-200 and miR-221/222 microRNA families: opposing effects on epithelial identity

@en

The miR-200 and miR-221/222 microRNA families: opposing effects on epithelial identity

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prefLabel

The miR-200 and miR-221/222 microRNA families: opposing effects on epithelial identity

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The miR-200 and miR-221/222 microRNA families: opposing effects on epithelial identity

@en

The miR-200 and miR-221/222 microRNA families: opposing effects on epithelial identity

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S10911-012-9244-6

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Journal of Mammary Gland Biology and Neoplasia

P1476

The miR-200 and miR-221/222 microRNA families: opposing effects on epithelial identity

@en

P2093

Dawn R. Cochrane

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Erin N. Howe

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Jennifer K. Richer

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miR-200 enhances mouse breast cancer cell colonization to form distant metastases

Loss of miR-200c: A Marker of Aggressiveness and Chemoresistance in Female Reproductive Cancers

The inhibition of the highly expressed miR-221 and miR-222 impairs the growth of prostate carcinoma xenografts in mice

MicroRNA-221 and microRNA-222 regulate gastric carcinoma cell proliferation and radioresistance by targeting PTEN

The miR-200 family inhibits epithelial-mesenchymal transition and cancer cell migration by direct targeting of E-cadherin transcriptional repressors ZEB1 and ZEB2

MicroRNAs: target recognition and regulatory functions

Loss of miR-200 inhibition of Suz12 leads to polycomb-mediated repression required for the formation and maintenance of cancer stem cells

Epithelial-mesenchymal transition in cancer: parallels between normal development and tumor progression

MicroRNA-221/222 negatively regulates estrogen receptor alpha and is associated with tamoxifen resistance in breast cancer

The miR-200 family determines the epithelial phenotype of cancer cells by targeting the E-cadherin repressors ZEB1 and ZEB2

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