Browse
Submit Data
Databases
API
Help

Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Expression data for human nasopharyngeal carcinoma cell line HK1 stimulated with EGF or TGF-Î² recombinant protein.

ABSTRACT: As regulators in gene expression, microRNAs take part in most biological process including cell differentiation, apoptosis, cell cycle and epithelial-to-mesenchymal transition (EMT). In order to evaluate their roles during the growth factors-induced EMT process, microRNA expression profile changes induced by EGF or TGF-Î² treatment on nasopharyngeal carcinoma cell line HK-1 cells were analyzed by means of the Affymetrix genome wide microarray system. Human nasopharyngeal carcinoma cell line HK-1 was starved for 12 hours before stimulation with EGF (50 ng/mL) or TGF-Î² (10ng/ml) or Control (PBS) for 36 hours in RPMI-1640 medium (with 1% serum) to establish the in vitro model of EMT. Total RNA were extracted and detected by AffymetrixÂ® GeneChipÂ® miRNA Arrays.

ORGANISM(S): Homo sapiens

SUBMITTER: Zailong Qin

PROVIDER: E-GEOD-64281 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

ACCESS DATA

Json Xml

Similar Datasets

Expression data for human nasopharyngeal carcinoma cell line HK1 stimulated with EGF or TGF-β recombinant protein.

Project description:As regulators in gene expression, microRNAs take part in most biological process including cell differentiation, apoptosis, cell cycle and epithelial-to-mesenchymal transition (EMT). In order to evaluate their roles during the growth factors-induced EMT process, microRNA expression profile changes induced by EGF or TGF-β treatment on nasopharyngeal carcinoma cell line HK-1 cells were analyzed by means of the Affymetrix genome wide microarray system.

2015-12-17 | GSE64281 | GEO

Direct regulation of alternative splicing by SMAD3 through interaction with PCBP1 is essential for the tumor-promoting role of TGF-beta

Project description:To assess the global impact of TGF-beta on alternative splicing, we conducted RNA-seq of total RNAs isolated from various lines of HeLa cells that were generated for this study and treated without or with TGF-beta and EGF. Using rMAT tool from the RNA-Seq data and annotation of transcripts in GTF format, we identified differential alternative splicing events between untreated and treated cell lines. Our study shows that the TGF-beta-mediated alternative splicing affects the protein products of a large number of genes enriched in pathways critical for EMT, cykeskeleton organization, and adherens junction signaling. PCBP1 was required for the most, if not all, alternative splicing events detected. SRA accession number: SRP061634, BioProject ID PRJNA290799. RNAs from Hela cells were treated with TGF-Î² and EGF, in triplicates and sequenced on HiSeq2000 with 2 samples pooled into one lane with Illumina TruSeq v3 chemistry.

2016-10-25 | E-GEOD-72419 | biostudies-arrayexpress

Overexpression of PHF8 promotes an EMT-related gene signature in MCF10A cells

Project description:PHF8 exerts distinct functions in different types of cancer. However, the mechanisms underlying its specific functions in each case remain obscure. To establish whether overexpression of PHF8 regulates the TGF-Î² induced the epithelial-mesenchymal transition (EMT), we treated MCF10A-Mock (control) and MCF10A-PHF8wt (overexpressing wild-type PHF8) cells with TGF-Î²1 for 0, 24, 48 and 72 hours and performed RNA-seq in biological duplicates. Our data indicated that EMT gene signatures were significantly enriched in MCF10A-PHF8 cells with TGF-Î²1 treatment at all time points, strongly indicating that PHF8 overexpression induces a sustained EMT signaling program. mRNA profiles of MCF10A-Mock (control) and MCF10A-PHF8 with TGF-Î²1 treatment for 0, 24, 48 and 72 hours were generated by RNA-seq, in duplicate, using HiSeq2500 instrument.

2016-10-26 | E-GEOD-74377 | biostudies-arrayexpress

Transcriptome sequencing of nasopharyngeal carcinoma model system (miRNA)

Project description:Nasopharyngeal carcinoma (NPC) is a prevalent malignancyt disease in Southeast Asia among the Chinese population. Aberrant regulation of transcripts has been implicated in many types of cancers including NPC. Herein, we characterized mRNA and miRNA transcriptomes by RNA sequencing (RNASeq) of NPC model systems. Matched total mRNA and small RNA of undifferentiated Epstein-Barr virus (EBV)-positive NPC xenograft X666 and its derived cell line C666, well-differentiated NPC cell line HK1, and the immortalized nasopharyngeal epithelial cell line NP460 have been sequenced by Solexa technology.

2014-02-05 | E-GEOD-54161 | biostudies-arrayexpress

Transcriptome sequencing of nasopharyngeal carcinoma model system (mRNA)

2014-02-05 | E-GEOD-54159 | biostudies-arrayexpress

TGF-Î² Tumor Suppression Through A Lethal EMT

Project description:TGF-Î² is a major tumor suppressor in gastrointestinal (GI) and squamous carcinomas, which exhibit frequent genetic inactivation of Smad4, a key TGF-Î² signaling component. Apoptosis is implicated as an important mediator of the tumor suppressive function of TGF-Î², although this process remains poorly understood. To address this long-standing question, we dissected the tumor suppressive action of TGF-Î² in naÃ¯ve pancreatic ductal adenocarcinoma (PDA) cells. Here we show that TGF-Î²/Smad4 signaling triggers an EMT in Kras-mutant pancreatic progenitor cells but turns this process into a trigger of apoptosis by converting the progenitor cell transcription factor Sox4 from an enforcer of epithelial progenitor identity into an activator of apoptosis. This occurs as a result of the EMT-linked repression of the endodermal master regulator Klf5, which cooperates with Sox4 to promote epithelial progenitor identity, and loss of which unmasks a latent apoptotic transcriptional program driven by Sox4. By losing Smad4, Kras-mutant PDA cells avoid this fate and instead use Sox4 as a TGF-Î²-dependent enforcer of the epithelial progenitor cell state. In this study, 16 RNA-Seq samples and 6 ChIP-Seq samples are included.

2016-02-24 | E-GEOD-72069 | biostudies-arrayexpress

Analysis of conditioned media cytokine levels of breast cancer cell lines

Project description:To identify the cytokines secreted by mesenchymal-like cancer cells that activate macrophages, the cytokine profiles of conditioned media from MCF7, MCF7 induced to undergo EMT by treatment of TGF-β, TNF-α and prolonged mammosphere culture, and MDA-MB-231 cells were analyzed by RayBio® Human Cytokine Antibody Array V. 5 samples. There are 5 groups: MCF7, MCF7 induced to undergo EMT by treatment of TGF-β (TGF-β-MCF7), TNF-α (TNF-α-MCF7), prolonged mammosphere culture (MCF7M), and MDA-MB-231 cells

2013-11-01 | E-GEOD-51938 | biostudies-arrayexpress

Vicious circle of LSD1 and TGF Î²1 promotes EMT of gastric cancer

Project description:Vicious circle of some key proteins is critical in the process of tumor development. Nevertheless, the mechanism of how the epigenetic modifiers are involved in was seldom reported and has not been clearly illustrated. We found the expression of lysine specific demethylase 1 (LSD1), the first identified histone lysine demethylase, is positively correlated with transforming growth factor beta 1 (TGF Î²1) in gastric cancer tissues and can be promoted by TGF Î²1 activated (p-EKR)-(NF-ÎºB)-p300 signaling pathway, which resulted in the progression of epithelial-mesenchymal transition (EMT) in human gastric cancer cells. On the other hand, abrogation of LSD1 leads to the down regulation of TGF Î²1 as well as the EMT. But in benign cells, this circle was blocked by TGF Î²1 induced inactivation of ERK, which suggested the distinct roles of TGF Î²1 against LSD1 in gastric cancer cells and benign cells. This vicious cycle may illustrate a novel mechanism for EMT in gastric cancer mediate by TGF Î²1 and LSD1 but not in benign cells and may serve as a new strategy for the prevention of EMT for gastric cancer. Nuclear extracts prepared from MGC803 cells stably expressing Lenti-CAS9-sgRNA-puro for LSD1 or empty vector were used in immunoprecipitation reactions with antibodies against H3K4me2 and H3K9me2. Sequencing libraries were prepared using the TruSeq DNA Sample Prep Kit (Illumina) and sequencing was performed on a HiSeq2000 (Illumina).

2016-07-19 | E-GEOD-84487 | biostudies-arrayexpress

Identification of miR-181a target genes in Epithelial Ovarian Cancer

Project description:We have identified a single miRNA, miR-181a, that can modulate TGF-Î² signaling to induce and maintain EMT, and effect further downstream events of tumour cell survival, altered response to chemotherapy, migration, invasion and dissemination in vivo. Our present study provides an understanding of how enhanced expression of miR-181a can confer malignant and invasive traits through the modulation of a canonical signaling pathway and a consequent maintenance of a mesenchymal state. Furthermore, inhibition of miR-181a led to a reversion of EMT and subsequent events through decreased TGF-Î² signaling. Our data confirmed Smad7 as a functional target through which TGF-Î²-mediated EMT occurs; re-expression of Smad7 lacking its 3'UTR was able to rescue miR-181a-mediated phenotypes, deeming Smad7 as a critical mediator of miR-181a-induced EMT. Other recent studies support the crucial role(s) that miRNAs play in mediating EMT and consequent aggressive disease traits. For example, the miR-106b-25 cluster has also been shown to target Smad7 and mediate TGF-Î²-induced EMT downstream to Six1 in breast cancer34. miR-9 directly targets E-cadherin and inhibition of miR-9 had led to an inhibition of metastasis35. Conversely, the miR-200 and -205 family was shown to target transcriptional repressors of E-cadherin, ZEB1 and SIP1, and re-expression of these miRNAs led to a mesenchymal-to-epithelial transition and prevented TGF-Î² -induced EMT36. A2780 ovarian cancer cell lines stably expressing either pBABE (control vector), p181a#1( clone 1 expressing miR-181a) or p181a#2( clone 2 expressing miR-181a)

2013-12-01 | E-GEOD-52077 | biostudies-arrayexpress

Human nasopharyngeal carcinoma

Project description:To uncover the oncogenic pathways of nasopharyngeal carcinoma, gene expression profiles of primary NPC cell strains and NPC-derived cell lines were conducted and analyzed in depth. Keywords: Oncogenesis Gene expression profiles of 9 primary NPC cell strains and 5 NPC-derived cell lines were analyzed. Forty Î¼g total RNA from one NPC sample was needed for a dye-swap experiment. Total RNA from 32 normal nasopharyngeal epithelial cell strains was pooled to serve as a universal reference.

2010-05-15 | E-GEOD-14262 | biostudies-arrayexpress

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