Project description:Three transcription factors KLF5, GATA4 and GATA6 are recurrently amplified in multiple gastric cancer cohorts, representing one type of lineage-survival oncogenes in gastric cancer. ChIP-Seq analysis of these three factors in multiple cell lines revealed that significant number of genomic sites are co-occupied by KLF5 and GATA4 and/or GATA6. Integrative analysis of ChIP-Seq and gene expression identified several targets of the three transcription factors in both cell lines and primary tumors, including HNF4A. These results suggest that KLF5, GATA4 and GATA6 interact and co-operate to regulate HNF4A and other genes to promote tumorigenesis in gastric cancer. Gene expression profiling of KLF5, GATA4 and GATA6 knock down in YCC3/AGS/KATOIII cells
Project description:The transcription factor Sox2 inhibits human gastric cancer growth and activates Sox2-related tumor surpressive genes in human gastric cancer cells. Conditional Sox2-overexpression in cells with a low Sox2 level demonstrated that the Sox2-regulated tumor surpressive genes demand on an enhanced Sox2 activity for better expression to work in human gastric cancer. Chromatin immunoprecipitation (ChIP) of Sox2 together with chromatin profiling by ChIP-on-chip analysis demonstrated that Sox2 directly activates the chromatin at promoters or putative enhancers of Sox2 target genes. Transcription factor Sox2 promoter array in MKN28 cells with Sox2 overexpression.
Project description:Transcriptional profiling of comparing control and GAPLINC knocking-down human gastric cancer cell lines. Goal was to determine the different gene expression between control and GAPLINC knocking-down human gastric cancer cell lines.
Project description:Molecules interacting with CasL 2 (MICAL2) belongs to a three-member family of multi-domain flavoprotein monooxygenase enzymes that catalyze actin oxidation-reduction reactions destabilizing F-actin in cytoskeletal dynamics. MICAL2 is over-expressed, being a negative prognostic factor, in aggressive gastric, kidney, prostate, bladder, breast and endometrial human cancer. MICAL2 is expressed in cancer-associated neo-angiogenic capillaries. The study of MICAL2 knock-down in endothelial cells shed light on the transcriptional impact of the gene on endothelial cell biology. To explore the transcriptional impact of the lack of Mical2 in endothelial cells, we performed genome-wide expression profiling of Mical2 knock-down SVEC4-10 (ATTC CRL-2181) cells (M2KD). Reference cells were: Mical3 knock-down (M3KD), obtained with same strategy; untreated SVEC4-10 cells ((WT), and cells transduced with insert-free viral vector (empty).
Project description:Transcriptional profiling of comparing control and GAPLINC stable knocking-down human gastric cancer cell lines. Goal was to determine the different gene expression between control and GAPLINC stable knocking-down human gastric cancer cell lines. Control and GAPLINC stable knocking-down human gastric cancer cell lines were prepared for RNA extraction and hybridization on Affymetrix microarrays.
Project description:We have generated Gas6 knock-down YTN16 cells using the shRNA system to specifically target Growth arrest-specific 6 (Gas6), a gene of interest in mouse gastric cancer cells. Additionally, we aimed to determine the differences in gene expression levels between YTN16 cells and YTN16 cells with Gas6 knock-down (shGas6) through RNA-sequencing analysis.
2023-06-20 | GSE234557 | GEO
Project description:Effect of knock down of LASP-1 on human breast cancer cells
Project description:Beta-catenin (CTNNB1) is a major component of Wnt signaling pathway and a crucial player in gastric cancer. To delineate the complex transcription program governed by CTNNB1 in gastric cancer cells, CTNNB1 was silenced in AGS, a commonly used Wnt signaling activated gastric cancer cell line and the resultant changes in genome-wide mRNA expression pattern was profiled using Affymetrix Human Gene 1.0 ST Array.
Project description:Beta-catenin is a major component of Wnt signaling pathway and a crucial player in gastric cancer. To delineate the complex transcription program governed by CTNNB1 in gastric cancer cells, CTNNB1 was silenced in YCC3, a commonly used Wnt signaling activated gastric cancer cell line and the resultant changes in genome-wide mRNA expression pattern was profiled using Affymetrix Human Gene 1.0 ST Array