Project description:Our data showed that EIF4EBP1, NINJ1, CLIC3, STMN3, SPINK4, CD44, GSN, PRSS23 et al. were strongly downregulated by miR-138-mimics in gastric cancer (GC) cell lines. Besides, miR-138-5p has a profound effect on EMT signaling and proliferation signaling. In the EMT signaling, miR-138-5p negatively regulates the expression of SOX4, VIM, TGFB1, BMP1, ECM1 and CXCL8; In the cell proliferation signaling, miR-138-5p could negatively regulates the expression of PCNA, RHOC and CCND3.
Project description:Increasing studies report that miR-194-5p plays a tumor suppressor role in gastric cancer (GC). Previous studies have revealed that miR-194 inhibited gastric cancer progression through different pathways by affecting the expression level of different target genes. For example, miR-194 have been reported to be able to regulate the expression of FOXM1, NR2F2, BMI1, SDAD1, RBX1, KDM5B, ZEB1 and AKT2 etc. It suggested that miR-194 may play complicated roles in GC. To figure out the mechanism of miR-194' tumor suppressor role in GC, we performed RNA sequencing in two different GC cell lines. Our studies showed that miR-194 tends to regulated target genes by binding on their 3' untranslated regions with either 7-mer-A1 or 7-mer-m8 or 8-mer. Approximately 138 genes were downregulated in both SGC7901 and BGC823 cell lines that transfected with miR-194-5p mimics compared to negative control siRNAs. Most of the downregulated genes have not reported yet.
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 previously showed that miR-138 can repress herpes simplex virus 1 (HSV-1) ICP0 expression by binding to ICP0 mRNA. However, in this study we found that miR-138 can also repress viral gene expression independent of ICP0. We did not find other confirmed viral targets of miR-138. Therefore we conducted these RNAseq experiments (in combination with PAR-CLIP experiments whose results are uploaded separately) to identify host targets of miR-138 in two cell lines to explain the ICP0-independent effects on HSV-1 gene expression.
Project description:In this study, we used miRNA sequencing to analyze and identify possible miRNAs that can be regulated by and UBE2CP3 in gastric cancer. The results showed that lncRNA UBE2CP3 overexpression decreased the expression of miR-138-5p. Due to miR-138-5p was able to target ITGA2 expression, and UBE2CP3 knockdown significantly downregulates ITGA2 expression, we speculated UBE2CP3 may positively regulate ITGA2 expression through sponging miR-138-5p in GC.
Project description:Like herpes simplex virus 1 (HSV-1) ICP0 mRNA, HSV-2 ICP0 mRNA is predicted to be targeted by a host neuron-specific microRNA, miR-138. This study was designed to confirm the interaction between HSV-2 ICP0 mRNA and miR-138, and to identify other potential viral and host targets of miR-138 during HSV-2 infection. We performed PAR-CLIP on HSV-2 infected 293T cells overexpressing miR-138 in comparisin to control 293T cells. The results confirmed ICP0 as miR-138's targets, and also identified some other potential viral and host targets of miR-138.
Project description:Using a miR-138 loss-of-function mouse model, a role for the brain enriched microRNA miR-138 in the regulation of inhibitory synaptic transmission and short-term memory formation was shown.
Project description:In other parts of this study we identified Foxc1 as a host target of miR-138 and found that Foxc1 can promote herpes simplex virus-1 (HSV-1) replication. To understand the mechanisms of this function, we performed an RNAseq experiment comparing vector (pcDNA) and pFoxchuman transfected Neuro-2a cells. After transfection, these cells were infected with HSV-1 for 5 hours at an MOI of 1 to identify viral genes regulated by Foxc1 as well as host genes.