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GoPubMed Proteins lists recent and important papers and reviews for proteins. Page last changed on 25 Jan 2016.

BMI1 polycomb ring finger oncogene

Top mentioned proteins: Polycomb, CAN, p16, EZH2, Histone
Papers using Bmi-1 antibodies
The Polycomb group protein EZH2 impairs DNA repair in breast epithelial cells
Hendzel Michael J. et al., In The Journal of Cell Biology, 2004
... Control and one of two different BMI1 shRNA plasmids were obtained from OriGene.
Papers on Bmi-1
The evolutionary landscape of PRC1 core components in green lineage.
Shen et al., Changsha, China. In Planta, 04 Feb 2016
We evaluated the origin of plant PRC1 RING-finger proteins (RING1 and BMI1) through comparing with the homologs in some representative unikonts and using BMI1- and RING1-like proteins as reciprocal outgroup, finding both PRC1 RING-finger proteins have the earliest origin in mosses, similar to LHP1.
Mitigation of arsenic-induced acquired cancer phenotype in prostate cancer stem cells by miR-143 restoration.
Tokar et al., United States. In Toxicol Appl Pharmacol, 22 Jan 2016
miR-143 restoration dysregulated the expression of SC/CSC self-renewal genes including NOTCH-1, BMI-1, OCT4 and ABCG2.
Expression of B cell-specific Moloney murine leukemia virus integration site 1 in vulvar squamous cell carcinoma and its effect on the biological behavior of A-431 cells.
Wen et al., Shenyang, China. In Oncol Lett, 31 Dec 2015
UNASSIGNED: The aim of the present study was to investigate the expression of B cell-specific Moloney murine leukemia virus integration site 1 (BMI-1) in vulvar squamous cell carcinoma (VSCC) and vulvar intraepithelial neoplasia (VIN).
BMI1 Regulation of Self-Renewal and Multipotency in Human Mesenchymal Stem Cells.
Nolta et al., Sacramento, United States. In Curr Stem Cell Res Ther, 31 Dec 2015
In the current studies we used loss-of-function and gain-of-function analyses in primary human MSCs to demonstrate that BMI1 is a critical regulator for self-renewal and multipotency in this interesting cell type.
BMI1, ALDH1A1, and CD133 Transcripts Connect Epithelial-Mesenchymal Transition to Cancer Stem Cells in Lung Carcinoma.
Cufer et al., Slovenia. In Stem Cells Int, 31 Dec 2015
In this study, we assessed mRNA expression levels of EMT-inducing transcription factors (BMI1, TWIST1), CSC (CD133, ALDH1A1), and epithelial (EpCAM) markers in primary tumor and whole blood samples obtained from 57 patients with operable non-small-cell lung cancer (NSCLC) as well as in circulating tumor cells (CTCs) of 13 patients with metastatic disease; then possible associations between marker expressions were evaluated.
Profiling the Behavior of Distinct Populations of Head and Neck Cancer Stem Cells.
Castilho et al., Ann Arbor, United States. In Cancers (basel), 31 Dec 2015
In addition, holospheres showed reduced proliferation (Ki67), hypoacetylation of histones, and increased expression of the BMI-1 epithelial stem cell marker, suggesting activation of stem cell programs.
Low adherent cancer cell subpopulations are enriched in tumorigenic and metastatic epithelial-to-mesenchymal transition-induced cancer stem-like cells.
Marchal et al., Granada, Spain. In Sci Rep, 31 Dec 2015
The TS subpopulation shows CXCL10, BMI-1 and OCT4 upregulation, differing also in the expression of several miRNAs involved in EMT and/or cell self-renewal such as miR-34a-5p, miR-34c-5p, miR-21-5p, miR-93-5p and miR-100-5p.
Overexpression and lack of copy number variation in the BMI-1 gene in human glioma.
Ghati Kasturirangan et al., Bengaluru, India. In Oncol Lett, Nov 2015
The B-cell-specific Moloney murine leukemia virus integration site 1 (BMI-1) gene is one of the major cancer stem cell factors responsible for treatment failure in glioma.
Immunosuppressive plasma cells impede T-cell-dependent immunogenic chemotherapy.
Karin et al., San Diego, United States. In Nature, Jun 2015
Our previous studies revealed that B cells recruited by the chemokine CXCL13 into prostate cancer tumours promote the progression of castrate-resistant prostate cancer by producing lymphotoxin, which activates an IκB kinase α (IKKα)-BMI1 module in prostate cancer stem cells.
MicroRNA Regulation of Human Breast Cancer Stem Cells.
Minami et al., Kōbe, Japan. In J Clin Med, 2014
The miRNAs and their clusters, such as the miR-200 clusters, miR-183 cluster, miR-221-222 cluster, let-7, miR-142 and miR-214, target the genes and pathways important for stem cell maintenance, such as the self-renewal gene BMI1, apoptosis, Wnt signaling, Notch signaling, and epithelial-to-mesenchymal transition.
Genetic alteration and misexpression of Polycomb group genes in hepatocellular carcinoma.
Xue et al., Xiamen, China. In Am J Cancer Res, 2014
Furthermore, Immunohistochemical staining revealed that the expression levels of CBX8 (in 53/123 samples) and BMI1 (in 60/130 samples) were markedly increased in human HCC specimens.
A functional genomic approach identifies FAL1 as an oncogenic long noncoding RNA that associates with BMI1 and represses p21 expression in cancer.
Zhang et al., Philadelphia, United States. In Cancer Cell, 2014
FAL1 associates with the epigenetic repressor BMI1 and regulates its stability in order to modulate the transcription of a number of genes including CDKN1A.
FAL1ing inside an amplicon.
Huarte et al., Pamplona, Spain. In Cancer Cell, 2014
FAL1 acts as an oncogene by stabilizing BMI1, which results in the repression of CDKN1A expression.
Expandable megakaryocyte cell lines enable clinically applicable generation of platelets from human induced pluripotent stem cells.
Eto et al., Kyoto, Japan. In Cell Stem Cell, 2014
This approach involves the establishment of stable immortalized megakaryocyte progenitor cell lines (imMKCLs) from PSC-derived hematopoietic progenitors through the overexpression of BMI1 and BCL-XL to respectively suppress senescence and apoptosis and the constrained overexpression of c-MYC to promote proliferation.
Self-renewal as a therapeutic target in human colorectal cancer.
O'Brien et al., Toronto, Canada. In Nat Med, 2014
Here we demonstrate that tumor formation and, more specifically, human colorectal CIC function are dependent on the canonical self-renewal regulator BMI-1.
Bmi1 is required for regeneration of the exocrine pancreas in mice.
Hebrok et al., San Francisco, United States. In Gastroenterology, 2012
Bmi1 contributes to regeneration of the exocrine pancreas after cerulein-induced injury through cell autonomous mechanisms, in part by regulating Cdkn2a expression, and non-cell autonomous mechanisms.
Prognostic relevance of c-Myc and BMI1 expression in patients with glioblastoma.
Larocca et al., Roma, Italy. In Am J Clin Pathol, 2012
We found that overexpression of c-Myc was significantly associated with that of BMI1, and that patients who harbored glioblastomas overexpressing c-Myc and BMI1 showed significantly longer overall survival.
Bmi1 facilitates primitive endoderm formation by stabilizing Gata6 during early mouse development.
Azuara et al., London, United Kingdom. In Genes Dev, 2012
Bmi1 overlaps with the nascent Gata6 and Nanog protein from the eight-cell stage onward before it preferentially cosegregates with Gata6 in primitive endoderm progenitors
Bmi1 confers resistance to oxidative stress on hematopoietic stem cells.
Iwama et al., Chiba, Japan. In Plos One, 2011
overexpression of Bmi1 confers resistance to stresses, particularly oxidative stress, onto hematopoietic stem cells. This enhances their regenerative capacity and suggests that Bmi1 is located downstream of ROS signaling and negatively regulated by it.
Bmi-1 siRNA inhibited ovarian cancer cell line growth and decreased telomerase activity.
Jin et al., Harbin, China. In Br J Biomed Sci, 2011
Bmi-1 siRNA has a role in inhibiting ovarian cancer cell line growth and decreasing telomerase activity
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