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Gene expression profiling of FUT8 knockdown CL1-5 cells

ABSTRACT: Overexpression of fucosyltransferase 8 (FUT8) is found in many cancers including liver, ovarian, thyroid, colorectal and non-small cell lung cancers. Unlike other FUTs which are functionally redundant, FUT8 is the only enzyme responsible for the alpha1,6-linked fucosylation (core fucosylation) by adding fucose to the innermost GlcNAc residue of an N-linked glycan. A growing body of evidence indicates that core fucosylation is important for regulating protein functions, such as EGFR, TGF beta receptor and integrins. To understand the downstream molecular events in response to the global alteration of core fucosylation during cancer progression, microarray analysis was employed to profile the changes in gene expression following FUT8 silencing. The genes significantly (2-fold, P<0.01) changed in CL1-5/shFUT8 cells were selected for functional annotations using a Gene Ontology database. The result revealed that many genes involved in cell adhesion, motility, growth, angiogenesis, and inflammation were under the control of core fucosylation. In this experiment, the gene expression profile of two stable FUT8 knockdown clones of CL1-5 cells, CL1-5/shFUT8-1 and CL1-5/shFUT8-2, were compare with CL1-5/Control cells. A total of eight samples were analyzed, including four CL1-5/Control vs. CL1-5/shFUT8-1 and four CL1-5/Control vs. C1-5/shFUT8-2. The biological replicates for each cell lines were four.

ORGANISM(S): Homo sapiens

SUBMITTER: Wong Chi-Huey

PROVIDER: S-ECPF-GEOD-42405 | biostudies-other |

REPOSITORIES: biostudies-other

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Gene expression profiling of FUT8 knockdown CL1-5 cells

Project description:Overexpression of fucosyltransferase 8 (FUT8) is found in many cancers including liver, ovarian, thyroid, colorectal and non-small cell lung cancers. Unlike other FUTs which are functionally redundant, FUT8 is the only enzyme responsible for the alpha1,6-linked fucosylation (core fucosylation) by adding fucose to the innermost GlcNAc residue of an N-linked glycan. A growing body of evidence indicates that core fucosylation is important for regulating protein functions, such as EGFR, TGF beta receptor and integrins. To understand the downstream molecular events in response to the global alteration of core fucosylation during cancer progression, microarray analysis was employed to profile the changes in gene expression following FUT8 silencing. The genes significantly (2-fold, P<0.01) changed in CL1-5/shFUT8 cells were selected for functional annotations using a Gene Ontology database. The result revealed that many genes involved in cell adhesion, motility, growth, angiogenesis, and inflammation were under the control of core fucosylation.

2012-12-07 | GSE42405 | GEO

Gene expression profiling of FUT8 knockdown CL1-5 cells

2012-12-07 | E-GEOD-42405 | biostudies-arrayexpress

Gene expression profiling of NB4 cells following knockdown of nucleostemin using DNA microarrays.

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| S-EPMC4918620 | biostudies-literature

Gene Expression Profiling of NFATc1-Knockdown in RAW 264.7 Cells: An Alternative Pathway for Macrophage Differentiation.

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Gene expression profiling in HSF1-knockdown human oral squamous cell carcinoma HSC-3 cells

Project description:Heat shock transcription factor 1 (HSF1) is recognized as the major regulator of the heat shock transcriptional response, and also plays a central role in the cellular functions of cancer cells. Here, to identify the molecular mechanism by which HSF1 regulates the proliferation of cancer cells, comparative gene expression analysis was performed with mock and HSF1-knockdown cells. Silencing of HSF1 in human oral squamous cell carcinoma HSC-3 cells was carried out by siRNA technology and the expression of HSF1 was confirmed by Western blotting. Gene expression was analyzed using GeneChip oligonucleotide microarrays and computational gene expression analysis tools. HSF1 knockdown significantly decreased the number of viable cells. Of the 54,675 probe sets analyzed, 221 probe sets were up-regulated and 423 probe sets were down-regulated by >2-fold in HSF1-knockdown cells. HSC-3 human oral squamous carcinoma cells were treated with siRNA for HSF1 or luciferase. Total RNA samples were prepared from the cells. Gene expression was analyzed by an Affymetrix GeneChip® system with a Human Genome U133-plus 2.0 array. Sample preparation for array hybridization was carried out as described in the manufacturer’s instructions.

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Gene expression profiling of MDA231, BT549, and SUM159PT cells after selumetinib treatment or DUSP4 siRNA knockdown

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