Project description:We have found expression of miR-146a up-regulated in gastric cancer. To identify new targets of miR-146a we profiled the transcriptome after miR-146a over-expression in the human gastric cancer cell line SNU638. SNU638 cells were transfected in triplicates with 50 nM miR-146a or control (siGlo) using Lipofectamine 2000. Total RNA was harvested 24 h after transfection using Trizol reagent. There are a total of six arrays included in this experiment, including three biological replicates of mRNA expression after miR-146a over-expression and three controls in SNU638 cells.
Project description:We found frequently down-regulation of microRNA-181c in human gastric cancer cases. To identify the potential target of miR-181c, we introduced miR-181c into a gastric cancer cell line KATO-III and analyzed significant changes of gene expression which was induced after introducing miR-181c. Keywords: dose response
Project description:Persistent colonization of the gastric mucosa by Helicobacter pylori (Hp) elicits chronic inflammation and aberrant epithelial cell proliferation, which increases the risk of gastric cancer. We examined the ability of microRNAs to modulate gastric cell proliferation in response to persistent Hp infection and found that epigenetic silencing of miR-210 plays a key role in gastric disease progression. Importantly, DNA methylation of the miR-210 gene was increased in Hp-positive human gastric biopsies as compared to Hp-negative controls. Moreover silencing of miR-210 in gastric epithelial cells promoted proliferation. We identified STMN1 and DIMT1 as miR-210 target genes and demonstrated that inhibition of miR-210 expression augmented cell proliferation by activating STMN1 and DIMT1. Together, our results highlight inflammation-induced epigenetic silencing of miR-210 as a mechanism of induction of chronic gastric diseases, including cancer, during Hp infection. To identify miR-210 targets in gastric cells, whole transcriptome analysis of AGS and MKN45 cells transfected with pre-miR-210 was conducted using Affymetrix GeneChip Human Genome U133 Plus 2.0 Array.
Project description:miR-483-5p and miR-551a were over-expressed in a colon cancer cell-line LvM3b to identify genes that are down-regulated by the miRNAs over-expression. Total RNA was isolated from miR-483-5p or miR-551a over-expressing LvM3b cells as well as control LvM3b cells.
Project description:miR-483-5p and miR-551a were over-expressed in a colon cancer cell-line LvM3b to identify genes that are down-regulated by the miRNAs over-expression. Total RNA was isolated from miR-483-5p or miR-551a over-expressing LvM3b cells as well as control LvM3b cells.
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
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:To identify targets of miR-550a-3-5p in human colon cancer, HCT116 cell line expressing miR-550a-3-5p was subjected to Illumina microarrays.
Project description:Genome-wide mRNA expression profiling was performed in AGS, gastric cancer cell line, upon miR-25 silencing. At 48 hours upon anti-miR-25-3p (miRNA inhibitor) and non-targeting control RNA transfection, the whole transcriptome profiling was performed in triplicates. The miR-25 silencing elevates the diffuse gastric cancer features like expression of COL1A2, expression of COL1A2 co-expressed genes, Epithelial to Mesenchymal Transition (EMT) and angiogenesis associated genes.