Browse
Submit Data
Databases
API
Help

Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

37 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Bmi-regulated miRNA expression pattern in head and neck cancers

ABSTRACT: The critical role of Bmi1 in promoting stem cell properties has been shown in different type of human cancers. Here, we established four stable clones to study Bmi-regulated miRNA expression patterns in head and neck caners. Bmi1-overexpressing cell lines (FaDu- Bmi1vs. FaDu-pcDNA3 cell line), and knock-down of Bmi1 cell lines (OECM1-sh-Bmi vs. OECM1-sh-Bmi1 cell lines) were established and used for analyzing miRNA expression patterms in Bmi-regulatory mechanism.

ORGANISM(S): Homo sapiens

SUBMITTER: Muh-Hwa Yang

PROVIDER: E-GEOD-31910 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

ACCESS DATA

Json Xml

Publications

Chromosome instability modulated by BMI1-AURKA signaling drives progression in head and neck cancer.

Chou Chun-Hung CH Yang Neng-Kai NK Liu Ting-Yun TY Tai Shyh-Kuan SK Hsu Dennis Shin-Shian DS Chen Ya-Wei YW Chen Yann-Jang YJ Chang Cheng-Chi CC Tzeng Cheng-Hwai CH Yang Muh-Hwa MH

Cancer research 20121130 2

Chromosomal instability (CIN) is widely considered a hallmark of cancer, but its precise roles in cancer stem cells (CSC) and malignant progression remain uncertain. BMI1 is a member of the Polycomb group of chromatin-modifier proteins that is essential for stem cell self-renewal. In human cancers, BMI1 overexpression drives stem-like properties associated with induction of epithelial-mesenchymal transition (EMT) that promotes invasion, metastasis, and poor prognosis. Here, we report that BMI1 m ...[more]

PMID: 23204235

Similar Datasets

Transcriptome drift of FADU after expression of HIF-1a, Twist1 or Bmi1

Project description:Expression of HIF-1a or Twist1 or Bmi1 in human hypopharyngeal cancer cell line FADU results in the drift of transcriptome profile from an epithelial cell-like signature to a mesenchymal stem cell-like signature. Stable transfection of pHA-HIF1a(dODD), pFLAG-Twist1 or pcDNA3-Bmi1 in FADU cell and analyzed the transcriptome by cDNA microarray. FADU transfected with pcDNA3.1 empty vector was used as a control of experiment.

2010-12-10 | E-GEOD-19406 | biostudies-arrayexpress

Bmi-regulated miRNA expression pattern in head and neck cancers

Project description:The critical role of Bmi1 in promoting stem cell properties has been shown in different type of human cancers. Here, we established four stable clones to study Bmi-regulated miRNA expression patterns in head and neck caners.

2013-02-11 | GSE31910 | GEO

BMI-1 promotes Ewing sarcoma tumorigenicity independent of CDKN2a-repression

Project description:Over-expression of the polycomb group gene BMI-1 is implicated in the pathogenesis of many human cancers. In this study, we investigate the role of BMI-1 as a functional oncogene in the Ewing’s Sarcoma Family of Tumors (ESFT), a highly aggressive group of bone and soft tissue tumors. Our data show that BMI-1 is highly expressed by the majority of primary ESFT and ESFT cell lines. However, in contrast to previous reports in other human cancer cell types, knockdown of BMI-1 in ESFT cell lines has no effect on cell survival. Instead, gain and loss of function studies in vitro and in vivo demonstrate that BMI-1 promotes the anchorage independent growth and tumorigenicity of ESFT. Importantly, we also find that modulation of BMI-1 alters the tumorigenicity of both p16-wild type and p16-null cell lines and that BMI-1-mediated effects on growth promotion are independent of CDKN2a repression. Gene expression profiling of ESFT cells following BMI-1 modulation reveals novel downstream effectors of BMI-1 function including key developmental, cell:cell and cell:matrix adhesion pathways. These data support a central role for BMI-1 in the pathogenesis of ESFT and reveal that p16-independent functions of BMI-1 are largely responsible for its oncogenic function in this tumor family. Keywords: Modification of BMI-1 expression in ESFT cell lines

2008-07-18 | GSE12064 | GEO

BMI Expression is Required for Pancreatic Cancer Progression

Project description:Pancreatic cancer is one of the deadliest human malignancies, with a survival rate less than 10%. Traditional modes of therapy have proven ineffective in the treatment of pancreatic cancer, highlighting the need to further understand the basic biology of the disease in order to identify new treatment modalities. Previously, our group showed that the epigenetic regulator Bmi1 is required for the initiation of pancreatic cancer in mice. In murine models of PDAC, mice lacking pancreatic Bmi1 expression do not develop precancerous lesions, despite oncogene expression. In this work, we sought to determine the role of Bmi1 in later stages of pancreatic tumor development. Using a CRISPR/Cas9 strategy, we deleted Bmi1 in primary human pancreatic caner cells and created clonal lines. When used in a subcutaenous tumor growth assay, those cells lacking BMI1 expression formed tumors that grew significantly smaller than controls. To query the mechanism of BMI1 action in pancreatic cancer growth, we used RNA sequencing to compare those pancreatic cancer cells with and without BMI1 expressed. This revealed that Bmi1 controls the gene expression of glycolysis and cell proliferation pathways, likely the reason for its requirement in pancreatic tumor growth. Overall, we found that Bmi1 is required in pancreatic tumor progression, and that it controls gene expression in both glycolysis and cell proliferation.

2023-06-30 | GSE149981 | GEO

The expression level of microRNA after knockdown of Twist1 or Bmi1

Project description:To screen the microRNA regulated by Twist1 and Bmi1 Establish stable transfectants of pSUPER-sh-Twist1 or pSUPER-sh-Bmi1 in OECM1 cells and analyze the miRNA expression level of by microRNA microarray. OECM1 transfected with pSUPER-sh-scr was used as a control experiment.

2013-02-11 | E-GEOD-29586 | biostudies-arrayexpress

Expression analysis of Pea3, Erm and Er81 overexpression in SH-SY5Y cell line

Project description:Investigation of whole genome gene expression level changes in SH-SY5Y cells transfected pCDNA3-Pea3, pCDNA3-Erm, and pCDNA3-Er81 cells compared to pCDNA3 transfected cells as a control.

2020-10-28 | E-MTAB-8473 | biostudies-arrayexpress

Differential gene expressions in dose-related radioresistant hypopharyngeal cancer cells

Project description:To explore the mechanisms underlying the radioresistance of hypopharyngeal carcinoma, we first established specifically radioresistant FaDu cell line (FaDu-RR cells) derived from FaDu cell lines by repeatedly exposing to different doses of ionizing radiation. Then, the aberrantly expressed mRNAs and IncRNAs were detected using microarrays and their bioinformatics were analyzed.

2020-08-11 | GSE102594 | GEO

Expression data of human hypopharyngeal tumor cells (FaDu)

Project description:FaDu cells were infected with lentivirus containing sh-luciferase plasmid to compared with cells infected with sh-G9a containing lentivirus. We performed microarray analysis to identify the genes possibly regulated by G9a in FaDu cells

2017-02-13 | GSE56330 | GEO

The Polycomb Group Protein Bmi-1 is essential for the growth of Multiple Myeloma cells

Project description:The RPMI-8226 human multiple myeloma cell line was stably infected with either a validated shRNA against BMI1 or a control shRNA. RNA was prepared from these lines, +/- doxycycline induction and at various time points post-induction. Samples were hybridized on the Affymetrix U133plus2 human genome expression microarray. The RPMI-8226 human multiple myeloma cell line was stably infected with either a validated shRNA against BMI1 or a control shRNA. RNA was prepared from these lines, +/- doxycycline induction and at various time points post-induction. Samples were hybridized on the Affymetrix U133plus2 human genome expression microarray.

2010-06-09 | E-GEOD-21912 | biostudies-arrayexpress

shRNA-mediated knock down of Bmi-1 and Mel-18 in medulloblastoma cells

Project description:Bmi-1 and Mel-18 are close structural homologues that belong to the polycomb group (PcG) of transcriptional regulators of homeotic gene expression in development. They are believed to stably maintain repression of gene expression by altering the state of chromatin at specific promoters. A number of clinical and experimental observations have also implicated Bmi-1 in tumorigenesis and stem cell maintenance. Bmi-1 overexpression or amplification has been observed in a number of human malignancies, particularly in B-cell lymphomas, medulloblastomas and breast cancer. We report here that shRNA-mediated knock-down of either Bmi-1 or Mel-18 in human medulloblastoma DAOY cells results in the inhibition of proliferation, loss of clonogenic survival and anchorage-independent growth, and suppression of xenograft tumor formation in nude mice. Furthermore, overexpression of both Bmi-1 and Mel-18 significantly increased clonogenic survival of Rat1 fibroblasts. In contrast, stable downregulation of Bmi-1 or Mel-18 alone did not affect the growth of SK-OV-3 or U2OS cancer cell lines or normal human WI38 fibroblasts. Gene expression analysis of shRNA-expressing DAOY cells has demonstrated a significant overlap in the Bmi-1- and Mel-18-regulated genes and revealed novel gene targets under their control. Taken together, these results suggest that Bmi-1 and Mel-18 might have overlapping functions in human tumorigenesis. Keywords: shRNA knock-down

2007-05-01 | GSE7578 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data