MiRNA expression profiling in PANC-1 cells treated with TGFb and additional PDAC lines
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ABSTRACT: miRNAs are known to be involved in PDAC tumourigenesis. However, not many have been investigated in the context of TGFb-induced EMT. To identify novel miRNAs involved in this response, we performed a miRNA profiling study in PANC-1 cells treated with TGFb and additional PDAC lines with epithelial or mesenchymal characteristics.
Project description:Gemcitabine has been a first-line therapeutic agent for pancreatic ductal adenocarcinoma (PDAC) pancreatic cancer; however, acquisition of resistance to gemcitabine remains a major challenge. We analyzed miRNAs expression profiles by array-based miRNAs analysis between gemcitabine–resistant (PANC-1/GEM) and parental PANC-1 cells.
Project description:Here we are using unbiased proteomic analysis based on affinity purification and MS to try to identify specific interactors of RBM42 in Panc-1 human PDAC cells.
Project description:Little is known about the role of FOXO3 and PDHA1 in PDAC. We performed microarrays to revealed the transcriptional change of a human pancreatic ductal adenocarcinoma (PDCA) cell line (Panc -1) to scr-siRNA, FOXO3-siRNA and PDHA1-siRNA in order to provide insight into the role of PDHA1 and FOXO3 in Panc-1 cells. Panc-1 Human PDCA cells were treated with scr-siRNA, FOXO3-siRNA and PDHA1-siRNA for 48 h and total RNA was extracted by using TRIzol Reagent. The microarray analysis was conducted on the Panc-1 cells expressing by using Agilent Microarray.
Project description:Little is known about the role of FOXO3 and PDHA1 in PDAC. We performed microarrays to revealed the transcriptional change of a human pancreatic ductal adenocarcinoma (PDCA) cell line (Panc -1) to scr-siRNA, FOXO3-siRNA and PDHA1-siRNA in order to provide insight into the role of PDHA1 and FOXO3 in Panc-1 cells.
Project description:To identify targets post-transcriptionally regulated by miR-100 and miR-125b, we have performed AGO2 RIP-seq and RNA-seq following overexpression of the two miRNAs in PANC-1 cells. In addition, we have carried out RNA-seq following TGFb stimulus to evaluate changes in gene expression driven by TGFb.
Project description:RNA-seq analysis was performed in PDAC patient-derived cell line PANC-1 (NC and METTL16-silenced) to analyze the expression of RNA levels after loss of METTL16.
Project description:Pancreatic cancer is a lethal diease with high tendency of metastasis. Howerver, the mechanisms of pancreatic cancer are sitill unclear. To explore the roles of N4-acetylation (ac4C) RNA modification and its involved N-Acetyltransferase 10 (NAT10) in pancreatic ductal adenocarcinoma (PDAC), we performed profiling by high throughput sequencing. In this study, we investigate the effects of NAT10 knockdown on N4-acetylcytidine (ac4C) modification in mRNA within PANC-1 cells using ac4C-seq. By employing RNA interference to specifically knock down NAT10 expression in PANC-1 cells, we aim to elucidate its impact on ac4C RNA modifications, which have been implicated in various cellular processes and cancer progression. Total RNA was extracted and mRNA was captured and treated with sodium borohydride (NaBH4) for detection of ac4C sites.Following library preparation, sequencing was performed on an Illumina Novaseq 6000 platform. Bioinformatics analyses identified significant changes in ac4C modification patterns due to NAT10 depletion. This dataset provides a valuable resource for further exploration of ac4C modifications in mRNA and their role in PDAC.
Project description:Screening of differentially expressed miRNAs in SW1990 and PANC-1 cells following GLI1 cDNA transfection. We independently transfected SW1990 and Panc-1 cells with Gli1 cDNA for mRNA and miRNA microarray analysis. The results unveiled significant differential expression patterns, with numerous miRNAs and mRNAs showing changes post-Gli1 transfection. Remarkably, miR-301a exhibited high expression in both SW1990 and Panc-1 cells transfected with Gli1 cDNA.
Project description:The dual tumor-suppressive and promoting function of TGFB signaling has made its targeting challenging. We hereby examined the effects of TGFB depletion by AVID200/BMS-986416(TGFB-TRAP), a TGFB ligand trap, on the tumor microenvironment of pancreatic ductal adenocarcinoma (PDAC) murine models with different organ-specific metastasis using single-nuclear RNA-sequencing (snRNA-seq)