Mel-18 acts as a tumor suppressor by repressing Bmi-1 expression and down-regulating Akt activity in breast cancer cells - Wikidata - awgldk - TriplyDB

Mel-18 acts as a tumor suppressor by repressing Bmi-1 expression and down-regulating Akt activity in breast cancer cells

Mel-18 acts as a tumor suppressor by repressing Bmi-1 expression and down-regulating Akt activity in breast cancer cells

http://www.wikidata.org/entity/Q24654211

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Loss of Mel-18 induces tumor angiogenesis through enhancing the activity and expression of HIF-1α mediated by the PTEN/PI3K/Akt pathway Molecular genetic analysis of Suppressor 2 of zeste identifies key functional domains BMI-1 promotes ewing sarcoma tumorigenicity independent of CDKN2A repression BMI1: A Biomarker of Hematologic Malignancies Su(z)2 antagonizes auto-repression of Myc in Drosophila, increasing Myc levels and subsequent trans-activation The synovial sarcoma-associated SYT-SSX2 oncogene antagonizes the polycomb complex protein Bmi1.BMI1 and Mel-18 oppositely regulate carcinogenesis and progression of gastric cancer.Polycomb CBX7 directly controls trimethylation of histone H3 at lysine 9 at the p16 locus.Expression of BMI-1 and Mel-18 in breast tissue--a diagnostic marker in patients with breast cancer USP22 maintains gastric cancer stem cell stemness and promotes gastric cancer progression by stabilizing BMI1 protein Polycomb group genes Psc and Su(z)2 restrict follicle stem cell self-renewal and extrusion by controlling canonical and noncanonical Wnt signaling MicroRNA-135a inhibits cell proliferation by targeting Bmi1 in pancreatic ductal adenocarcinoma.Deletion analysis of BMI1 oncoprotein identifies its negative regulatory domain microRNA-141 regulates BMI1 expression and induces senescence in human diploid fibroblasts.Oncogenic role of the chromobox protein CBX7 in gastric cancer.Polycomb group proteins: multi-faceted regulators of somatic stem cells and cancer.Identification and characterization of Bmi-1-responding element within the human p16 promoter.Expression and clinicopathological significance of Mel-18 and Bmi-1 mRNA in gastric carcinoma.Polycomb genes expression as a predictor of poor clinical outcome in children with medulloblastoma.Polycomb group genes Psc and Su(z)2 maintain somatic stem cell identity and activity in Drosophila.Bmi-1 promotes invasion and metastasis, and its elevated expression is correlated with an advanced stage of breast cancer PLK1 inhibition down-regulates polycomb group protein BMI1 via modulation of the miR-200c/141 cluster.βTrCP regulates BMI1 protein turnover via ubiquitination and degradation.Systematic detection of putative tumor suppressor genes through the combined use of exome and transcriptome sequencing MicroRNA-31 is a transcriptional target of histone deacetylase inhibitors and a regulator of cellular senescence MYCN and MYC regulate tumor proliferation and tumorigenesis directly through BMI1 in human neuroblastomas.MEL-18 loss mediates estrogen receptor-α downregulation and hormone independence.Increased Levels of Circulating and Tissue mRNAs of Oct-4, Sox-2, Bmi-1 and Nanog is ESCC Patients: Potential Tool for Minimally Invasive Cancer Diagnosis.Akt-mediated phosphorylation of Bmi1 modulates its oncogenic potential, E3 ligase activity, and DNA damage repair activity in mouse prostate cancer.Depletion of the chromatin remodeler CHD4 sensitizes AML blasts to genotoxic agents and reduces tumor formation Bmi-1: At the crossroads of physiological and pathological biology.A positive feedback loop regulates the expression of polycomb group protein BMI1 via WNT signaling pathway.Bmi-1 cooperates with H-Ras to transform human mammary epithelial cells via dysregulation of multiple growth-regulatory pathways.Association between Bmi1 and clinicopathological status of esophageal squamous cell carcinoma Antitumor activity and inhibitory effects on cancer stem cell-like properties of Adeno-associated virus (AAV) -mediated Bmi-1 interference driven by Bmi-1 promoter for gastric cancer.Bmi-1 regulates stem cell-like properties of gastric cancer cells via modulating miRNAs BMI1 cooperates with H-RAS to induce an aggressive breast cancer phenotype with brain metastases.A miR-200c/141-BMI1 autoregulatory loop regulates oncogenic activity of BMI1 in cancer cells.Distinct population of highly malignant cells in a head and neck squamous cell carcinoma cell line established by xenograft model.The polycomb group protein Bmi-1 represses the tumor suppressor PTEN and induces epithelial-mesenchymal transition in human nasopharyngeal epithelial cells.

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Mel-18 acts as a tumor suppressor by repressing Bmi-1 expression and down-regulating Akt activity in breast cancer cells

http://www.wikidata.org/entity/Q24654211

description

2007 nî lūn-bûn

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2007 թուականի Յունիսին հրատարակուած գիտական յօդուած

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2007 թվականի հունիսին հրատարակված գիտական հոդված

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2007年の論文

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2007年論文

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2007年論文

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2007年論文

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2007年論文

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2007年論文

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2007年论文

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name

Mel-18 acts as a tumor suppres ...... ctivity in breast cancer cells

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Mel-18 acts as a tumor suppres ...... ctivity in breast cancer cells

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Mel-18 acts as a tumor suppres ...... ctivity in breast cancer cells

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Mel-18 acts as a tumor suppres ...... ctivity in breast cancer cells

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Mel-18 acts as a tumor suppres ...... ctivity in breast cancer cells

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Mel-18 acts as a tumor suppres ...... ctivity in breast cancer cells

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Mel-18 acts as a tumor suppres ...... ctivity in breast cancer cells

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Mel-18 acts as a tumor suppres ...... ctivity in breast cancer cells

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Cancer Research

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Ajay Yadav

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Bao-Hong Guo

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Goberdhan P Dimri

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Li-Bing Song

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Mu-Sheng Zeng

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Wei-Jian Guo

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P2860

Microarray analysis identifies a death-from-cancer signature predicting therapy failure in patients with multiple types of cancer

Control of the replicative life span of human fibroblasts by p16 and the polycomb protein Bmi-1

EZH2 is a marker of aggressive breast cancer and promotes neoplastic transformation of breast epithelial cells

Mel-18, a polycomb group protein, regulates cell proliferation and senescence via transcriptional repression of Bmi-1 and c-Myc oncoproteins

Hedgehog signaling and Bmi-1 regulate self-renewal of normal and malignant human mammary stem cells

Multiple roles of the PI3K/PKB (Akt) pathway in cell cycle progression

The oncogene and Polycomb-group gene bmi-1 regulates cell proliferation and senescence through the ink4a locus

The Bmi-1 oncogene induces telomerase activity and immortalizes human mammary epithelial cells.

Stem cells and cancer; the polycomb connection.

Implication of polycomb members Bmi-1, Mel-18, and Hpc-2 in the regulation of p16INK4a, p14ARF, h-TERT, and c-Myc expression in primary breast carcinomas.

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