Gene expression changes in gastric and colon cancer cell lines after RHOA knockdown.
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE110237 | GEO | 2021/02/01
REPOSITORIES: GEO
Similar Datasets
Project description:Stable knockdown of NET1, a RhoGEF, was achieved in AGS Gastric Cancer cells. This gene is known to be overexpressed in the disease. Knockdown was achieved using lentiviral shRNA particles. Gene expression was compared between knockdown and scrambled shRNA treated control cells. Cells were treated with and without LPA, a known activator of RhoA.
2011-01-02 | GSE26309 | GEO
Project description:Stable knockdown of NET1, a RhoGEF, was achieved in AGS Gastric Cancer cells. This gene is known to be overexpressed in the disease. Knockdown was achieved using lentiviral shRNA particles. Gene expression was compared between knockdown and scrambled shRNA treated control cells. Cells were treated with and without LPA, a known activator of RhoA. Three distinct cell lines were used in this study (all AGS cells); (i) Non Target cell (NT) stably expressing non targetting shRNA (ii) 63 and (iii) 65; the latter two are stable NET1 knockdown cells and are seperatly transduced with separate NET1 targetting shRNA particles. Cells were treated with and without 10microM LPA for 4 hr. Experimental replicates were performed for each treatment (A & B), RNA was prepared from each and seperatly hybridised to U133A arrays.
2011-01-02 | E-GEOD-26309 | biostudies-arrayexpress
Project description:Previously, we designed pharmacologically optimized inhibitor RHOA, a major signaling hub in gastric cancer (GC), the fourth most common cause of death in the world. Here, based on that previous work, we perform the lead optimization and design new RHOA inhibitors for greater anti-GC potency. Two of these compounds, JK-206 and -312 inhibit cell viability and migration of GC cell lines. Furthermore, through our transcriptomics analysis of JK-206 treatment in GC cells, we revealed that pharmacologic inhibition of RHOA was associated with inhibition of mitogenic pathway, including BIRC5. Thus, RHOA→BIRC5 can be regarded as a new therapeutic strategy in GC, possibly regulating proliferation and migration in oncogenic mechanisms.
2022-03-24 | GSE188908 | GEO
Project description:The transcription factor MIST1 is required for final maturation of secretory cells of diverse tissues, including gastric digestive-enzyme secreting zymogenic (chief) cells (ZCs). Here, we show that MIST1 directly activates RAB26, RAB3D and several other genes. Experiment Overall Design: We used microarrays to determine genes upregulated following transient MIST1 transfection. Two gastric cell lines were used: HGC-27 and AGS. Three chips were generated from each cell line: parental (untransfected), GFP+empty vector (a control for effects of transfection), and GFP+MIST1. The latter two chips were generated from cells flow sorted based on GFP fluorescence to isolate cells with high levels of transfection. Chips were analyzed by dChip to identify genes expressed in both MIST1-transfected cell populations relative to their respective controls in multiple Boolean 'AND' comparisons.
2010-01-30 | E-GEOD-16924 | biostudies-arrayexpress
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. ChIP-Seq experiments of KLF5, GATA4 and GATA6 were performed in three gastric cancer cell lines YCC3, AGS and KATOIII
2014-09-05 | E-GEOD-51705 | biostudies-arrayexpress
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
2014-09-05 | E-GEOD-51704 | biostudies-arrayexpress
Project description:MicroRNA microarray profiling analysis was performed on human gastric cancer HGC cells after RACK1 silenced or not
2016-03-01 | E-MTAB-3484 | biostudies-arrayexpress
Project description:Rho family small GTPases serve as molecular switches in the regulation of diverse cellular functions including actin cytoskeleton remodeling, cell migration, gene transcription, and cell proliferation. Importantly, Rho overexpression is frequently seen in many carcinomas. However, published studies have almost invariably utilized immortal or tumorigenic cell lines to study Rho GTPase functions and there are no studies on the potential of Rho small GTPase to overcome senescence checkpoints and induce preneoplastic transformation of human mammary epithelial cells (hMECs). We found that ectopic expression of wild-type RhoA as well as a constitutively-active RhoA mutant (G14V) in primary hMEC strains led to their immortalization and preneoplastic transformation. Significantly, RhoA-T37A mutant, known to be incapable of interacting with many well known Rho-effectors ,was also capable of immortalizing hMECs.Our results demonstrate that RhoA can induce the preneoplastic transformation of hMECs by altering multiple pathways linked cellular transformation and breast cancer. Through microarray analysis, we want to identify genes and pathways linked to RhoA induced hMECs immortalization. Experiment Overall Design: 4 samples, in triplicate analyses per sample.
2008-10-26 | E-GEOD-12917 | biostudies-arrayexpress
Project description:The small GTPase RhoA regulates a variety of cellular processes, including cell motility, proliferation, survival and permeability. In addition, there are reports suggesting that the RhoA-ROCK axis plays a role in VEGF-mediated angiogenesis, whereas other work has shown opposite effects. To elucidate this conflicting data, we examined HUVEC and HCAEC after stable overexpression (lentiviral transduction) of constitutively active (G14V/Q63L), dominant-negative (T19N), or wild-type RhoA using a variety of in vitro angiogenesis assays (proliferation, migration, tube formation, angiogenic sprouting, endothelial cell viability) and a HUVEC xenograft assay in immune incompetent NSGTM mice in vivo. We observed that expression of active as well as wild-type RhoA but not expression of dominant-negative RhoA significantly increased endothelial cell death as well as inhibited endothelial cell proliferation, migration, tube formation and angiogenic sprouting of endothelial cells in vitro and reduced HUVEC-related angiogenesis in vivo. Inhibition of RhoA by C3 transferase antagonized inhibitory RhoA effects and strongly enhanced VEGF-induced angiogenic sprouting in control-treated cells. In contrast, inhibition of RhoA effectors ROCK1/2 and LIMK1/2 had no significant effect on RhoA-related effects, but again increased angiogenic sprouting and migration of control-treated cells. In line with these data, VEGF did not activate RhoA in HUVEC as measured by a FRET-based biosensor. Furthermore, global transcriptome and subsequent bioinformatic gene ontology (GO) enrichment analyses revealed that constitutively active RhoA induces a differentially expressed gene pattern that is enriched for GO biological process terms such as mitotic nuclear division, cell proliferation, cell motility and cell adhesion and includes a significant decrease in VEGFR-2 and NOS3 expression. Thus, our data demonstrate that increased RhoA activity has the potential to trigger endothelial dysfunction and anti-angiogenic effects independently of its well-characterized downstream effectors ROCK and LIMK.
2022-07-06 | GSE182806 | GEO
Project description:Using mice with a keratinocyte-restricted deletion of the RhoA gene, we explored its role in the regulation of gene expression in vivo and in vitro RNA was isolated from RhoA-null or wildtype keratinocytes, in two different conditions, freshly isolated (in vivo) or cultured (in vitro), using the RNeasy kit (Qiagen, Germany). Hybridization to GeneChip Mouse Genome 430 2.0 Array (Affymetrix, Santa Clara, CA) was carried out at the Copenhagen University Hospital Microarray Center using standard protocols. 2 biological replicates were analyzed for each in vivo genotype (2 samples from RhoA-null, 2 from wildtype), while 3 replicates for each in vitro genotype.
2015-01-07 | E-GEOD-64714 | biostudies-arrayexpress