Rorc disruption in human FG pancreatic cancer cells
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA522288 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR8571770.fastq.gz | Fastqsanger.gz | |||
| SRR8571765.fastq.gz | Fastqsanger.gz | |||
| SRR8571766.fastq.gz | Fastqsanger.gz | |||
| SRR8571767.fastq.gz | Fastqsanger.gz | |||
| SRR8571768.fastq.gz | Fastqsanger.gz |
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Project description:Rorc disruption in human FG pancreatic cancer cells
2019-02-15 | GSE126537 | GEO
Project description:Purpose: Core 3 derived glycans, a major type of O-glycan expressed by normal epithelial cells of the gastrointestinal tract, are downregulated during malignancy, because of loss of expression of functional β3-N-acetylglucosaminyltransferase-6 (core 3 synthase). We investigated the expression of core 3 synthase in normal pancreas and pancreatic cancer and evaluated the biological effects of re-expressing core 3 synthase in pancreatic cancer cells that had lost expression. Experimental Design: We determined that pancreatic tumors and tumor cell lines have lost expression of core 3 synthase. We therefore re-expressed in human pancreatic cancer cells (Capan-2 and FG) to investigate the contribution of core 3 glycans to malignant progression. Results: Pancreatic cancer cells expressing core 3 synthase showed reduced in vitro cell proliferation, migration and invasion compared with vector control cells. Expression of core 3 O-glycans induced altered expression of β1 integrin, decreased activation of focal adhesion kinase, led to the down regulation of expression of several genes including REG1α and FGFR3, and altered lamellipodia formation. The addition of a GlcNAc residue by core 3 synthase leads to the extension of the tumor associated Tn structure on MUC1. Orthotopic injection of FG cells expressing core 3 synthase into the pancreas of nude mice produced significantly smaller tumors and decreased metastasis to the surrounding tissues compared to vector control FG cells. Conclusions: These findings indicate that expression of core 3 derived O-glycans in pancreatic cancer cells suppresses tumor growth and metastasis through modulation of glycosylation of mucins and other cell surface and extracellular matrix proteins. Two-condition experiment, Core 3 synthase stable expression (C3) vs. vector control (PLVX) cells. Biological replicates: 3 Core 3 synthase stable expression, 3 vector control, independently grown and harvested. One replicate per array.
2012-11-21 | E-GEOD-42417 | biostudies-arrayexpress
Project description:Purpose: Core 3 derived glycans, a major type of O-glycan expressed by normal epithelial cells of the gastrointestinal tract, are downregulated during malignancy, because of loss of expression of functional β3-N-acetylglucosaminyltransferase-6 (core 3 synthase). We investigated the expression of core 3 synthase in normal pancreas and pancreatic cancer and evaluated the biological effects of re-expressing core 3 synthase in pancreatic cancer cells that had lost expression. Experimental Design: We determined that pancreatic tumors and tumor cell lines have lost expression of core 3 synthase. We therefore re-expressed in human pancreatic cancer cells (Capan-2 and FG) to investigate the contribution of core 3 glycans to malignant progression. Results: Pancreatic cancer cells expressing core 3 synthase showed reduced in vitro cell proliferation, migration and invasion compared with vector control cells. Expression of core 3 O-glycans induced altered expression of β1 integrin, decreased activation of focal adhesion kinase, led to the down regulation of expression of several genes including REG1α and FGFR3, and altered lamellipodia formation. The addition of a GlcNAc residue by core 3 synthase leads to the extension of the tumor associated Tn structure on MUC1. Orthotopic injection of FG cells expressing core 3 synthase into the pancreas of nude mice produced significantly smaller tumors and decreased metastasis to the surrounding tissues compared to vector control FG cells. Conclusions: These findings indicate that expression of core 3 derived O-glycans in pancreatic cancer cells suppresses tumor growth and metastasis through modulation of glycosylation of mucins and other cell surface and extracellular matrix proteins.
2012-11-21 | GSE42417 | GEO
Project description:Two pancreatic cancer cell lines with different metastatic and growth potential were compared under hypoxic conditions and under normal atmospheric oxygen pressure. The FG cell lines shows very few metastases and slow growth in mouse xenograft models. L3.6pl, derived from FG by cycles re-implantation of metastatic cells obtained after orthotopic tumor growth in nude mice, shows high motility, aggressive growth and very high metastatic potential By comparison of the two cell lines under different oxygen concentration we tried to simulate in vivo conditions of tumors at different growth stages. Differentially expressed genes and transcription factor regulating coexpressed genes identified by SOTA clustering were used to identify key genes that define metastatic potential of pancreatic cancer cells Keywords: 2+2 factorial design 12 samples, two cell lines * two culture conditions(oxygen pressure) * three replicates
2010-09-30 | E-GEOD-9350 | biostudies-arrayexpress
Project description:Background: Non-small cell lung cancer (NSCLC) accounts for 81% of all cases of lung cancer and they are often fatal because 60% of the patients are diagnosed at an advanced stage. Besides the need for earlier diagnosis, there is a great need for additional effective therapies. In this work we investigated the feasibility of a lung cancer progression mouse model, mimicking features of human aggressive NSCLC cancer, as biological reservoir for potential therapeutic targets and biomarkers. Results:RNA-seq profiling was performed on total RNA extracted from lungs of 30 week-old p53R172HM-bM-^HM-^Fg/KrasG12D and wild type mice to detect fusion genes and gene/exon-level differential expression associated to the increase of tumor mass. Fusion events were not detected in p53R172HM-bM-^HM-^Fg/KrasG12D tumors. Differential expression at exon-level detected 33 genes with differential exon usage. The study provides a complete transcription overview of the p53R172HM-bM-^HM-^Fg/KrasG12D mouse NSCLC model Lung mRNA profiles of 30-week old wild type (WT) and p53R172HM-bM-^HM-^Fg/KrasG12D mice were generated by deep sequencing, in duplicate using Illumina HiSeq2000.
2013-09-25 | E-GEOD-51144 | biostudies-arrayexpress
Project description:DMS-MaPseq of RORC reporters and endogeneous RORC locus
| PRJNA1105608 | ENA
Project description:Two pancreatic cancer cell lines with different metastatic and growth potential were compared under hypoxic conditions and under normal atmospheric oxygen pressure. The FG cell lines shows very few metastases and slow growth in mouse xenograft models. L3.6pl, derived from FG by cycles re-implantation of metastatic cells obtained after orthotopic tumor growth in nude mice, shows high motility, aggressive growth and very high metastatic potential By comparison of the two cell lines under different oxygen concentration we tried to simulate in vivo conditions of tumors at different growth stages. Differentially expressed genes and transcription factor regulating coexpressed genes identified by SOTA clustering were used to identify key genes that define metastatic potential of pancreatic cancer cells Keywords: 2+2 factorial design
2010-09-30 | GSE9350 | GEO