Browse
Submit Data
Databases
API
Help

Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

39 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

RNAi profiling of human fascin knockdown esophageal squamous carcinoma cells

ABSTRACT: Fascin, an actin-binding protein, is upregulated in a variety of cancers, including esophageal squamous cell carcinoma (ESCC) and is proposed to function in cellular growth, mobility and invasiveness. Nonetheless, the molecular mechanisms through which fascin expression contributes to the proliferation and invasiveness of ESCC are unknown. To address this issue and to identify genes and biological pathways associated with fascin expression, a genome-wide gene expression analysis was performed on a fascin RNAi-depleted cell line and a corresponding ESCC cell line previously determined to express high levels of fascin. Experiment Overall Design: We used cDNA microarrays to identify genes that were differentially expressed upon fascin knockdown. For this purpose, we selected PSF8 (Fascin siRNA-depleted cell) and PSC(blank vector control cell ), two ESCC cell lines recently established in our laboratory. Total RNA from PSF8 cells and PSC cells was prepared for use with Affymetrix U133 cDNA microarrays.

ORGANISM(S): Homo sapiens

SUBMITTER: Enmin Li

PROVIDER: E-GEOD-11373 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

ACCESS DATA

Json Xml

Similar Datasets

Gene expression profile analysis for the Fascin knockdown esophageal squamous carcinoma cells

Project description:Fascin, an actin-binding protein, is upregulated in a variety of cancers, including esophageal squamous cell carcinoma (ESCC) and is proposed to function in cellular growth, mobility and invasiveness. Nonetheless, the molecular mechanisms through which fascin expression contributes to the proliferation and invasiveness of ESCC are unknown. To address this issue and to identify genes and biological pathways associated with fascin expression, a genome-wide gene expression analysis was performed on a fascin RNAi-depleted cell line and a corresponding ESCC cell line previously determined to express high levels of fascin. Keywords: cell type comparison

2008-05-08 | GSE11373 | GEO

A novel Lysyl oxidase like 2 alternative splicing LOXL2 â³e13 in esophageal squamous carcinoma cells

Project description:A novel alternative splicing isoform of LOXL2 â³e13 was expressed ubiquitously in all cell lines and ESCC tissues. In contrast to the impaired deamination enzymatic activity compared with full length LOXL2, LOXL2 â³e13 showed an enhanced ability to promote cell mobility and invasiveness in ESCC cells than full length LOXL2 through a different mechanism. We used cDNA microarrays to identify genes that were differentially expressed upon LOXL2 â³ e13 overexpressed. For this purpose, we selected LOXL2 â³ e13, WT and empty vector control transfeced ESCC KYSE150 cell lines. Total RNA was extracted,compare the gene expression patterns between LOXL2 â³e13, LOXL2 WT and empty vector control transfected cells through the Genechip Primeview Human Gene Expression Array.

2016-07-03 | E-GEOD-53676 | biostudies-arrayexpress

A novel Lysyl oxidase like 2 alternative splicing LOXL2 △e13 in esophageal squamous carcinoma cells

Project description:A novel alternative splicing isoform of LOXL2 △e13 was expressed ubiquitously in all cell lines and ESCC tissues. In contrast to the impaired deamination enzymatic activity compared with full length LOXL2, LOXL2 △e13 showed an enhanced ability to promote cell mobility and invasiveness in ESCC cells than full length LOXL2 through a different mechanism.

2016-01-01 | GSE53676 | GEO

Gene expression profile for NGAL overexpression in esophageal squamous carcinoma cell

Project description:Neutrophil gelatinase associated lipocalin (NGAL), also known as oncogene 24p3, uterocalin, siderocalin or lipocalin 2 (Lcn2), is a member of the lipocalin family. Elevated NGAL involves various functions in malignant cells, even sometimes the conclusions were controversial. NGAL inhibits apoptosis in thyroid cancer and decrease invasion and angiogenesis in pancreatic cancer, but it increase proliferation and metastasis in breast and colon cancer. Nonetheless, the molecular functions and mechanisms of NGAL in ESCC are unknown. To address these issues and to identify genes and biological pathways associated with NGAL functions and mechanism, NGAL was overexpressed by pcDNA3.0 plasmid in ESCC cell line EC109 with an empty plasmid as a control, these two cells were applied for mRNA expression profile analyses to find the differentially expressed genes. Plasmids of pcDNA3.0-NGAL and pcDNA3.0 were transfected into ESCC cell line EC109, respectively. Stable transfected cell clones were selected by G418. The overexpression of NGAL protein was confirmed by western blot. Total RNAs from NGAL overexpressed cells and control cells were extracted for Agilent whole genome oligo microarray. A dye flip was performed for duplicate.

2014-05-14 | E-GEOD-57630 | biostudies-arrayexpress

lncRNA profiles enable prognosis prediction and subtyping for esophageal squamous cell carcinoma

Project description:AC007128.1, a long non-coding RNA, was upregulated in both ESCC tissues and cells, and associated with poor prognosis in ESCC. AC007128.1 can promote migration and invasion in ESCC cell lines. By RNA-sequencing analysis, we observed the significant changes of genes important in AC007128.1-depleted cells. We generated two KYSE150 cell lines stably transduced with either a sh-NC lentiviral construct or a shRNA lentiviral construct designed to target AC007128.1 RNA to investigate the consequences on the gene expression profile of AC007128.1 knockdown in KYSE150 cells.

2021-02-24 | GSE167345 | GEO

Esophageal Cancer Project

Project description:Esophageal cancer is one of the most aggressive cancers and the sixth leading cause of cancer death worldwide. Approximately 70% of the global esophageal cancers occur in China and over 90% histopathological forms of this disease are esophageal squamous cell carcinoma (ESCC). Currently, there are limited clinical approaches for early diagnosis and treatment for ESCC, resulting in a 10% 5-year survival rate for the patients. Meanwhile, the full repertoire of genomic events leading to the pathogenesis of ESCC remains unclear. Here we show a comprehensive genomic analysis in 158 ESCC cases, as part of the International Cancer Genome Consortium (ICGC) Research Projects (http://icgc.org/icgc/cgp/72/371/1001734). We conducted whole-genome sequencing in 17 ESCC cases and whole-exome sequencing in 71 cases, of which 53 cases and additional 70 ESCC cases were subjected to array comparative genomic hybridization (a-CGH) analysis. We conducted whole-genome sequencing in 17 ESCC cases and whole-exome sequencing in 71 cases, of which 53 cases and additional 70 ESCC cases were subjected to array comparative genomic hybridization (a-CGH) analysis.

2014-03-11 | E-GEOD-54995 | biostudies-arrayexpress

METTL3 mediated m6A mRNA modification promotes esophageal cancer initiation and progression via Notch signaling pathway

Project description:Esophageal cancer is a lethal malignancy with high mortality rate, while the molecular mechanisms underlying esophageal cancer pathogenesis are stillis poorly understood. Here we found that the N6-methyladenosine (m6A) methyltransferase METTL3 is significantly up-regulated in esophageal squamous cell carcinoma (ESCC) and associated with poor patient prognosis. Depletion of METTL3 results in decreased ESCC growth and progression in vitro and in vivo. We further established ESCC initiation and progression models using Mettl3 conditional knockout mouse and revealed that Mettl3 mediated m6A modification is essential for promotes ESCC initiation and progression in vivo. Moreover, using METTL3 overexpression ESCC cell model and Mettl3 conditional knockin mouse model, we demonstrated the critical function of Mettl3 in promoting in vivo ESCC tumorigenesis in vitro and in vivo. Mechanistically, Mettl3 catalyzed m6A modification promotes NOTCH1 expression and the activation of Notch signaling pathway. Forced activation of Notch signaling pathway successfully rescues the growth, migration and invasion capacities of METTL3 depleted ESCC cells. Our data uncovered important mechanistical insights underlying ESCC tumorigenesis and provided molecular basis for the development of novel strategies for ESCC diagnosis and treatment.

2021-09-15 | GSE179267 | GEO

Global gene expression profiling and validation in esophageal squamous cell carcinoma (ESCC)

Project description:Esophageal squamous cell carcinoma (ESCC) is an aggressive tumor with poor prognosis. Understanding molecular changes in ESCC should improve identification of risk factors in molecular subtypes and provide potential targets for early detection and therapy. To better characterize molecular changes in ESCC, we followed up a previous cDNA array study with additional discovery and confirmatory studies in new ESCC cases using alternative methods. We profiled global gene expression (Affymetrix U133A/B chip) for discovery and confirmation, and validated selected dysregulated genes with additional RNA (qRT-PCR, N=51) or protein studies (immunohistochemistry [IHC] of tumor tissue microarray [TMA], N=275).We also found genes associated with survival. The dysregulated genes should aid in identifying risk factors in ESCC, as well as potential targets for early detection, and outcome prediction and therapy.

2010-09-01 | GSE23400 | GEO

Global gene expression profiling and validation in esophageal squamous cell carcinoma (ESCC)

2010-09-01 | E-GEOD-23400 | biostudies-arrayexpress

Gene expression profile for NGAL overexpression in esophageal squamous carcinoma cell

2014-05-14 | GSE57630 | GEO