Functional evidence that the self-renewal gene NANOG regulates human tumor development - Wikidata - awgldk - TriplyDB

Functional evidence that the self-renewal gene NANOG regulates human tumor development

Functional evidence that the self-renewal gene NANOG regulates human tumor development

http://www.wikidata.org/entity/Q35891426

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The microRNA miR-34a inhibits prostate cancer stem cells and metastasis by directly repressing CD44 The PSA(-/lo) prostate cancer cell population harbors self-renewing long-term tumor-propagating cells that resist castration.Cancer Stem Cells and Epithelial-to-Mesenchymal Transition (EMT)-Phenotypic Cells: Are They Cousins or Twins?Sox2 is an androgen receptor-repressed gene that promotes castration-resistant prostate cancer Expression of evolutionarily novel genes in tumors The Androgen Receptor Bridges Stem Cell-Associated Signaling Nodes in Prostate Stem Cells The network of pluripotency, epithelial-mesenchymal transition, and prognosis of breast cancer Insights into Chemoresistance of Prostate Cancer Androgen receptor and prostate cancer stem cells: biological mechanisms and clinical implications Twists in views on RB functions in cellular signaling, metabolism and stem cells Insights into the Nanog gene: A propeller for stemness in primitive stem cells The role of NANOG transcriptional factor in the development of malignant phenotype of cancer cells Concise Review: NANOG in Cancer Stem Cells and Tumor Development: An Update and Outstanding Questions Embryonic NANOG activity defines colorectal cancer stem cells and modulates through AP1- and TCF-dependent mechanisms Drug-tolerant cancer cells show reduced tumor-initiating capacity: depletion of CD44 cells and evidence for epigenetic mechanisms Nanog1 in NTERA-2 and recombinant NanogP8 from somatic cancer cells adopt multiple protein conformations and migrate at multiple M.W species Registered report: the microRNA miR-34a inhibits prostate cancer stem cells and metastasis by directly repressing CD44 NANOGP8: evolution of a human-specific retro-oncogene Stress granule-associated protein G3BP2 regulates breast tumor initiation.NANOG promotes cancer stem cell characteristics and prostate cancer resistance to androgen deprivation.Reciprocal regulation by TLR4 and TGF-β in tumor-initiating stem-like cells.Identification of DPPA4 and DPPA2 as a novel family of pluripotency-related oncogenes.Pluripotent transcription factors possess distinct roles in normal versus transformed human stem cells.Epithelial to mesenchymal transition is mechanistically linked with stem cell signatures in prostate cancer cells Phosphorylation of Nanog is essential to regulate Bmi1 and promote tumorigenesis.Genomic profiling of tumor initiating prostatospheres.C-terminal truncated hepatitis B virus X protein regulates tumorigenicity, self-renewal and drug resistance via STAT3/Nanog signaling pathway.Emerging role of nanog in tumorigenesis and cancer stem cells.Snail1 induces epithelial-to-mesenchymal transition and tumor initiating stem cell characteristics NANOG regulates glioma stem cells and is essential in vivo acting in a cross-functional network with GLI1 and p53.The dietary bioflavonoid quercetin synergizes with epigallocathechin gallate (EGCG) to inhibit prostate cancer stem cell characteristics, invasion, migration and epithelial-mesenchymal transition.Prostate cancer cell lines under hypoxia exhibit greater stem-like properties.Transcription factors Foxa1 and Foxa2 are required for adult dopamine neurons maintenance.3-O-methylfunicone, from Penicillium pinophilum, is a selective inhibitor of breast cancer stem cells.Distinct microRNA expression profiles in prostate cancer stem/progenitor cells and tumor-suppressive functions of let-7.A 1536-well quantitative high-throughput screen to identify compounds targeting cancer stem cells.Pseudogene in cancer: real functions and promising signature.Regulation of NANOG in cancer cells.CRISPR/Cas9-mediated gene knockout of NANOG and NANOGP8 decreases the malignant potential of prostate cancer cells TALEN-mediated Nanog disruption results in less invasiveness, more chemosensitivity and reversal of EMT in Hela cells.

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Functional evidence that the self-renewal gene NANOG regulates human tumor development

http://www.wikidata.org/entity/Q35891426

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2009 nî lūn-bûn

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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年论文

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2009年论文

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2009年论文

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name

Functional evidence that the self-renewal gene NANOG regulates human tumor development

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Functional evidence that the self-renewal gene NANOG regulates human tumor development

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type

label

Functional evidence that the self-renewal gene NANOG regulates human tumor development

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Functional evidence that the self-renewal gene NANOG regulates human tumor development

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prefLabel

Functional evidence that the self-renewal gene NANOG regulates human tumor development

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Functional evidence that the self-renewal gene NANOG regulates human tumor development

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Functional evidence that the self-renewal gene NANOG regulates human tumor development

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Can Liu

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Dean G Tang

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Grace Choy

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Holm Zaehres

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Lubna Patrawala

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Mark Badeaux

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Tammy Calhoun-Davis

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P2860

Core transcriptional regulatory circuitry in human embryonic stem cells

Identification, cloning and expression analysis of the pluripotency promoting Nanog genes in mouse and human

Identification and characterization of ovarian cancer-initiating cells from primary human tumors

Oct4 expression is not required for mouse somatic stem cell self-renewal

The homeoprotein Nanog is required for maintenance of pluripotency in mouse epiblast and ES cells

Functional expression cloning of Nanog, a pluripotency sustaining factor in embryonic stem cells

High-efficiency RNA interference in human embryonic stem cells

Eleven daughters of NANOG

A protein interaction network for pluripotency of embryonic stem cells

Cancer stem cells in solid tumours: accumulating evidence and unresolved questions

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993-1005

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10.1002/STEM.29

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5

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27

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George Q. Daley

Collene R Jeter

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24402015

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molecular medicine

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3327393

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