Counterbalance between RB inactivation and miR-17-92 overexpression in reactive oxygen species and DNA damage induction in lung cancers - Wikidata - awgldk - TriplyDB

Counterbalance between RB inactivation and miR-17-92 overexpression in reactive oxygen species and DNA damage induction in lung cancers

Counterbalance between RB inactivation and miR-17-92 overexpression in reactive oxygen species and DNA damage induction in lung cancers

http://www.wikidata.org/entity/Q28251838

about

miR-17, miR-19b, miR-20a, and miR-106a are down-regulated in human aging Feud or Friend? The Role of the miR-17-92 Cluster in Tumorigenesis miR-17-92 cluster: ups and downs in cancer and aging Insights into the Regulatory Role of Non-coding RNAs in Cancer Metabolism Role of Exosomal Noncoding RNAs in Lung Carcinogenesis MicroRNAs, DNA Damage Response, and Cancer Treatment The miR-19a/b family positively regulates cardiomyocyte hypertrophy by targeting atrogin-1 and MuRF-1 MicroRNAs as therapeutic targets for lung cancer miR-17* suppresses tumorigenicity of prostate cancer by inhibiting mitochondrial antioxidant enzymes MicroRNAs As Biomarkers For Clinical Features Of Lung Cancer MicroRNA in lung cancer.Effects of miR-19b overexpression on proliferation, differentiation, apoptosis and Wnt/β-catenin signaling pathway in P19 cell model of cardiac differentiation in vitro.miRConnect 2.0: identification of oncogenic, antagonistic miRNA families in three human cancers The regulatory and predictive functions of miR-17 and miR-92 families on cisplatin resistance of non-small cell lung cancer Mechanistic Roles of Noncoding RNAs in Lung Cancer Biology and Their Clinical Implications Detection of Exosomal miRNAs in the Plasma of Melanoma Patients.MicroRNA-92a negatively regulates Toll-like receptor (TLR)-triggered inflammatory response in macrophages by targeting MKK4 kinase.Signaling mechanism(s) of reactive oxygen species in Epithelial-Mesenchymal Transition reminiscent of cancer stem cells in tumor progression.The roles of microRNAs in tumorigenesis and angiogenesis.Prognostic, therapeutic and diagnostic potential of microRNAs in non-small cell lung cancer.miRNAs in lung cancer: large roles for small players.MicroRNA as a novel drug target for cancer therapy.MicroRNAs and lung cancers: from pathogenesis to clinical implications The microRNA-17-92 family of microRNA clusters in development and disease.microRNA regulation of cell viability and drug sensitivity in lung cancer.H2AX a promising biomarker for lung cancer: a review.miRNA expression profiles associated with diagnosis and prognosis in lung cancer.The role of microRNAs in the regulation of apoptosis in lung cancer and its application in cancer treatment MicroRNAs in lung cancer.New insights into lung development and diseases: the role of microRNAs.Non-small-cell lung cancer and miRNAs: novel biomarkers and promising tools for treatment.Mitochondrial miRNA (MitomiR): a new player in cardiovascular health.MicroRNA-17-5p inhibits proliferation and triggers apoptosis in non-small cell lung cancer by targeting transforming growth factor β receptor 2.Splicing regulator SLU7 preserves survival of hepatocellular carcinoma cells and other solid tumors via oncogenic miR-17-92 cluster expression.miR-342-3p regulates MYC transcriptional activity via direct repression of E2F1 in human lung cancer.Enterococcus faecalis Infection and Reactive Oxygen Species Down-Regulates the miR-17-92 Cluster in Gastric Adenocarcinoma Cell Culture.Selective killing of lung cancer cells by miRNA-506 molecule through inhibiting NF-κB p65 to evoke reactive oxygen species generation and p53 activation.Bortezomib induces apoptosis of endometrial cancer cells through microRNA-17-5p by targeting p21.MicroRNA 17-92 expressed by a transposone-based vector changes expression level of cell-cycle-related genes.MicroRNA-192 targeting retinoblastoma 1 inhibits cell proliferation and induces cell apoptosis in lung cancer cells.

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P2860

Counterbalance between RB inactivation and miR-17-92 overexpression in reactive oxygen species and DNA damage induction in lung cancers

http://www.wikidata.org/entity/Q28251838

description

2009 nî lūn-bûn

@nan

2009 թուականի Սեպտեմբերին հրատարակուած գիտական յօդուած

@hyw

2009 թվականի սեպտեմբերին հրատարակված գիտական հոդված

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2009年の論文

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2009年論文

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2009年論文

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2009年論文

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2009年論文

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2009年論文

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2009年论文

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name

Counterbalance between RB inac ...... mage induction in lung cancers

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Counterbalance between RB inac ...... mage induction in lung cancers

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Counterbalance between RB inac ...... mage induction in lung cancers

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Counterbalance between RB inac ...... mage induction in lung cancers

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Counterbalance between RB inac ...... mage induction in lung cancers

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Counterbalance between RB inac ...... mage induction in lung cancers

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Counterbalance between RB inac ...... mage induction in lung cancers

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Counterbalance between RB inac ...... mage induction in lung cancers

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M Suzuki

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N Sugito

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P2860

Targeted deletion reveals essential and overlapping functions of the miR-17 through 92 family of miRNA clusters

miR-17 and miR-20a temper an E2F1-induced G1 checkpoint to regulate cell cycle progression

Transgenic over-expression of the microRNA miR-17-92 cluster promotes proliferation and inhibits differentiation of lung epithelial progenitor cells

RAS is regulated by the let-7 microRNA family

c-Myc-regulated microRNAs modulate E2F1 expression

Reduced expression of the let-7 microRNAs in human lung cancers in association with shortened postoperative survival

E2F1-regulated microRNAs impair TGFbeta-dependent cell-cycle arrest and apoptosis in gastric cancer

A polycistronic microRNA cluster, miR-17-92, is overexpressed in human lung cancers and enhances cell proliferation

Alterations of the PPP2R1B gene in human lung and colon cancer

Identification of hypoxia-inducible factor-1 alpha as a novel target for miR-17-92 microRNA cluster

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3371-3379

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10.1038/ONC.2009.201

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38

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28

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Takashi Takahashi

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