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GoPubMed Proteins lists recent and important papers and reviews for proteins. Page last changed on 23 May 2015.

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
MicroRNA-218 inhibits the proliferation and metastasis of esophageal squamous cell carcinoma cells by targeting BMI1.
Wu et al., Suzhou, China. In Int J Mol Med, 21 Jun 2015
Western blot analysis and luciferase reporter assay revealed that miR-218 decreased BMI1 expression by binding to the putative binding sites in its 3'-untranslated region (3'-UTR).
MicroRNA-218 inhibits bladder cancer cell proliferation, migration, and invasion by targeting BMI-1.
Lu et al., Nanjing, China. In Tumour Biol, 14 Jun 2015
Luciferase reporter assay showed that BMI-1 was a direct target of miR-218.
Immunosuppressive plasma cells impede T-cell-dependent immunogenic chemotherapy.
Karin et al., San Diego, United States. In Nature, 07 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-429 suppresses cell proliferation, epithelial-mesenchymal transition, and metastasis by direct targeting of BMI1 and E2F3 in renal cell carcinoma.
Chen et al., Zhanjiang, China. In Urol Oncol, 04 Jun 2015
miR-429 was shown to directly target the 3' untranslated regions of B-cell-specific Moloney murine leukemia virus insertion site 1 (BMI1) and E2F transcription factor 3 (E2F3) transcripts, regulating their expression, as well as that of the downstream epithelial-to-mesenchymal transition markers E-cadherin, N-cadherin, vimentin, p14, and p16.
Bmi1 is required for the initiation of pancreatic cancer through an Ink4a-independent mechanism.
Pasca di Magliano et al., Xi'an, China. In Carcinogenesis, 04 Jun 2015
BMI1, a component of the Polycomb protein family, plays a key role in these processes by controlling the histone ubiquitination and long-term repression of multiple genomic loci.
Cancer stem cells in oesophageal squamous cell carcinoma: Identification, prognostic and treatment perspectives.
Lam et al., Gold Coast, Australia. In Crit Rev Oncol Hematol, 16 May 2015
It has also been demonstrated that stem cell markers like ALDH1, HIWI, Oct3/4, ABCG2, SOX2, SALL4, BMI-1, NANOG, CD133 and podoplanin are associated with patient's prognosis, pathological stages, cancer recurrence and therapy resistance.
Anticancer Effect of AntiMalarial Artemisinin Compounds.
Das, Dibrugarh, India. In Ann Med Health Sci Res, Mar 2015
Artemisinins seem to regulate key factors such as nuclear factor-kappa B, survivin, NOXA, hypoxia-inducible factor-1α, and BMI-1, involving multiple pathways that may affect drug response, drug interactions, drug resistance, and associated parameters upon normal cells.
Clinical Implications of Intestinal Stem Cell Markers in Colorectal Cancer.
Troelsen et al., Denmark. In Clin Colorectal Cancer, Jan 2015
This review provides an overview of the intestinal stem cell markers leucine-rich repeat-containing G-protein-coupled receptor 5 (LGR5), B cell-specific Moloney murine leukemia virus insertion site 1 (BMI1), Musashi1 (MSI1), and sex-determining region y-box 9 (SOX9) and their implications in human CRC.
Prognostic value of tumor suppressors in osteosarcoma before and after neoadjuvant chemotherapy.
Fuchs et al., Zürich, Switzerland. In Bmc Cancer, Dec 2014
We performed immunohistochemical stainings of P53, P16, maspin, PTEN, BMI1 and Ki67, characterized the subcellular localization and related staining outcome with chemotherapy response and overall survival.
FAL1ing inside an amplicon.
Huarte et al., Pamplona, Spain. In Cancer Cell, Oct 2014
FAL1 acts as an oncogene by stabilizing BMI1, which results in the repression of CDKN1A expression.
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, Oct 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.
Novel therapeutic targets for pancreatic cancer.
Chen et al., Hong Kong, Hong Kong. In World J Gastroenterol, Sep 2014
In order to give a better understanding of the current findings and to seek the direction in future pancreatic cancer research; in this review we will focus on targets suppressing tumour metastatsis and progression, KRAS activated downstream effectors, the relationship of Notch signaling and Nodal/Activin signaling with pancreatic cancer cells, the current findings of non-coding RNAs in inhibiting pancreatic cancer cell proliferation, brief discussion in transcription remodeling by epigenetic modifiers (e.g., HDAC, BMI1, EZH2) and the plausible therapeutic applications of cancer stem cell and hyaluronan in tumour environment.
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, May 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.
Genetic Modeling of PIM Proteins in Cancer: Proviral Tagging and Cooperation with Oncogenes, Tumor Suppressor Genes, and Carcinogens.
Blanco-Aparicio et al., Madrid, Spain. In Front Oncol, 2013
The use of retroviral insertional mutagenesis and refined approaches such as complementation tagging has allowed the identification of myc, pim, and a third group of genes (including bmi1 and gfi1) as complementing genes in lymphomagenesis.
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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