Similar Datasets
Project description:RHOA is a recurrently mutated gene in diffuse-type gastric cancer, whose molecular influence in gastric cancer has not been well uncovered. We aimed to clarify the contribution of RHOA to pro-oncogenesis to improve the understanding of the role of RHOA as a therapeutic target. We performed microarray analysis after RHOA knockdown for HGC-27, AGS, CCK-81, and SW948.
2021-02-01 | GSE110237 | GEO
Project description:The study was undertaken to identify microRNAs differently expressed by intestinal type of gastric cancer using miRNA microarray. The miRNA expression in the intestinal type of gastric cancer depending on H. pylori infection suggest that different gastric cancer pathogenesis could be exist between H. pylori-positive and -negative gastric cancer. Total RNA was extracted from cancerous region and non-cancerous regions in formalin fixed paraffin embedded tissues of intestinal type gastric cancer patients who were H. pylori-positive (n=8) or -negative (n=8). Corresponding author: Nayoung Kim, M.D., Department of Internal Medicine, Seoul National University Bundang Hospital (Tel., +82-31-787-7008; e-mail, nayoungkim49@empas.com).
2014-01-25 | E-GEOD-54397 | biostudies-arrayexpress
Project description:The study was undertaken to identify microRNAs differently expressed by intestinal type of gastric cancer using miRNA microarray. The miRNA expression in the intestinal type of gastric cancer depending on H. pylori infection suggest that different gastric cancer pathogenesis could be exist between H. pylori-positive and -negative gastric cancer.
2014-01-25 | GSE54397 | GEO
Project description:Previously, we identified Ras homologous A (RHOA) as a major signalling hub in gastric cancer (GC), the third-most common cause of cancer death in the world, prompting us to rationally design an efficacious inhibitor of this oncogenic GTPase. Here, based on that previous work, we extend those computational analyses, and in silico modeling approaches, to further pharmacologically optimize anti-RHOA hydrazide derivatives for greater anti-GC potency. Two of these, JK-136 and JK-139, potently inhibited cell viability and migration/invasion of GC cell lines, and mouse xenografts, diversely expressing RHOA. Moreover, JK-136’s binding affinity for RHOA was >140-fold greater than Rhosin, a nonclinical RHOA inhibitor. Network analysis of JK-136/139-associated transcriptomes showed different functional contexts, compared to those following treatment with Rhosin. We strongly assert that identifying and targeting oncogenic signalling hubs, such as RHOA, represents an emerging strategy for the design, characterization, and translation of new antineoplastics, against gastric and other cancers.
2020-05-25 | GSE135068 | GEO
Project description:Regions of recurrent genomic amplification and deletion are frequently observed in primary gastric cancers (GC). However, identifying specific oncogenes and tumor suppressor genes within these regions can be challenging, as they often cover tens to hundreds of genes. Here, we combined high-resolution array-based comparative genomic hybridization (aCGH) with gene expression profiling to target genes lying within focal high-level amplifications in GC cell lines, and identified RAB23 as an amplified and overexpressed Chr 6p11p12 gene in Hs746T cells. High RAB23 protein expression was also observed in some lines lacking RAB23 amplification, suggesting additional mechanisms besides gene amplification for up-regulating RAB23. siRNA silencing of RAB23 reduced the invasive potential of both amplified and nonamplified GC cell lines. RAB23 gene amplifications were observed in 13% of primary gastric carcinomas. In two independent patient cohorts, RAB23 transcript and protein expression was significantly associated with diffuse-type gastric cancer (dGC) compared to intestinal-type gastric cancer (iGC), providing further evidence that dGC and iGC likely represent two molecularly distinct tumor types. Our study demonstrates that investigating focal chromosomal amplifications by combining highresolution aCGH with expression profiling is a powerful general strategy for identifying novel cancer genes in recurrent regions of chromosomal aberration. Keywords: gastric cancer cell lines, comparative genomic hybridization, gene expression profiling
2008-12-29 | GSE10611 | GEO
Project description:Regions of recurrent genomic amplification and deletion are frequently observed in primary gastric cancers (GC). However, identifying specific oncogenes and tumor suppressor genes within these regions can be challenging, as they often cover tens to hundreds of genes. Here, we combined high-resolution array-based comparative genomic hybridization (aCGH) with gene expression profiling to target genes lying within focal high-level amplifications in GC cell lines, and identified RAB23 as an amplified and overexpressed Chr 6p11p12 gene in Hs746T cells. High RAB23 protein expression was also observed in some lines lacking RAB23 amplification, suggesting additional mechanisms besides gene amplification for up-regulating RAB23. siRNA silencing of RAB23 reduced the invasive potential of both amplified and nonamplified GC cell lines. RAB23 gene amplifications were observed in 13% of primary gastric carcinomas. In two independent patient cohorts, RAB23 transcript and protein expression was significantly associated with diffuse-type gastric cancer (dGC) compared to intestinal-type gastric cancer (iGC), providing further evidence that dGC and iGC likely represent two molecularly distinct tumor types. Our study demonstrates that investigating focal chromosomal amplifications by combining highresolution aCGH with expression profiling is a powerful general strategy for identifying novel cancer genes in recurrent regions of chromosomal aberration. Keywords: gastric cancer cell lines, comparative genomic hybridization, gene expression profiling Affy 100K SNP profiling and 32K BAC Array profiling for 7 Gastric Cancer Cell Lines
2010-05-14 | E-GEOD-10611 | biostudies-arrayexpress
Project description:Genome wide DNA methylation profiling of gastric cancer cell lines. The Illumina Goldengate DNA methylation Beadchip was used to obtain DNA methylation profiles across 1,505 CpG CpGs in 20 gastric cancer cell lines.
2012-05-03 | GSE29499 | GEO
Project description:Gene expression changes in gastric and colon cancer cell lines after RHOA knockdown.
| PRJNA433229 | ENA
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:Genome wide DNA methylation profiling of gastric cancer cell lines. The Illumina Goldengate DNA methylation Beadchip was used to obtain DNA methylation profiles across 1,505 CpG CpGs in 20 gastric cancer cell lines. Bisulphite converted DNA from the 20 gastric cancer cell lines were hybridised to the Illumina Goldengate Methylation Beadchip
2012-05-02 | E-GEOD-29499 | biostudies-arrayexpress