Homo sapiens
Ontology highlight
ABSTRACT:
OTHER RELATED OMICS DATASETS IN: E-GEOD-19279E-GEOD-19280E-GEOD-19278
PROVIDER: PRJNA123891 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:S100P is a metastasis-associated gene that facilitates transendothelial migration of pancreatic cancer cells [HG-U133_Plus_2]
2015-08-06 | E-GEOD-19278 | ExpressionAtlas
Project description:S100P is a metastasis-associated gene that facilitates transendothelial migration of pancreatic cancer cells [HG-U133_Plus_2]
| PRJNA123889 | ENA
Project description:S100P is a metastasis-associated gene that facilitates transendothelial migration of pancreatic cancer cells [HG-U133B]
| PRJNA123893 | ENA
Project description:We and others have shown that S100P is highly upregulated during the progression of pancreatic cancer. We used microarrays to look at the target genes regulated by S100P in the pancreatic cancer cell line Panc1. Keywords: Gene overexpression We generated stable cell lines by introducing control vector pcDNA3.1/V5-His or S100P-overexpressing vector pcDNA3.1/S100P-V5-His into the pancreatic cancer cell line Panc1, single cell clones were then isolated. RNA was extracted and hybridized on Affymetrix microarrays. We looked for new target genes regulated by S100P.
2013-08-15 | E-GEOD-19278 | biostudies-arrayexpress
Project description:We and others have shown that S100P is highly upregulated during the progression of pancreatic cancer. We used microarrays to look at the target genes regulated by S100P in the pancreatic cancer cell line Panc1. Keywords: Gene overexpression
2013-08-15 | GSE19278 | GEO
Project description:HDAC2 facilitates pancreatic cancer metastasis
| PRJEB47385 | ENA
Project description:Metastatic colonization involves cancer cell lodgment or adherence in the microvasculature and subsequent migration of those cells across the endothelium into a secondary organ site. To study this process further, we analyzed transendothelial migration of human PC-3 prostate cancer cells in vitro. We isolated a subpopulation of cells, TEM4-18, that crossed an endothelial barrier more efficiently, but surprisingly, were less invasive than parental PC-3 cells in other contexts in vitro. Importantly, TEM4-18 cells were more aggressive than PC-3 cells in a murine metastatic colonization model. Microarray and FACS analysis of these cells showed that the expression of many genes previously associated with leukocyte trafficking and cancer cell extravasation were either unchanged or down-regulated. TEM4-18 cells exhibited characteristic molecular markers of an epithelial-to-mesenchymal transition (EMT), including frank loss of E-cadherin expression and upregulation of the E-cadherin repressor ZEB1. Silencing ZEB1 in TEM4-18 cells resulted in increased E-cadherin and reduced transendothelial migration. TEM4-18 cells also express N-cadherin, which was found to be necessary, but not sufficient for increased transendothelial migration. Our results extend the role of EMT in metastasis to transendothelial migration and implicate ZEB1 and N-cadherin in this process in prostate cancer cells. Experiment Overall Design: We wanted to compare the expression profiles of cells that had undergone transendothelial migration. The parental, and reference cell line, PC-3 was plated onto a confluent human microvascular endothelial cell line from the lung and allowed to migrate across this monolayer. A new cell line, TEM4-18, was isolated from this experiment. We also performed this experiment a second time to isolate a biological replicate of the TEM4-18 cell line, termed TEM2-5. All 3 cell lines, PC-3, TEM4-18, and TEM2-5 are analyzed as replicates in this experiment for a total of 6 samples in this microarray. Both TEM4-18 and TEM2-5 were then compared to PC-3 cells for changes in gene expression.
2009-01-25 | E-GEOD-14405 | biostudies-arrayexpress
Project description:Metastatic colonization involves cancer cell lodgment or adherence in the microvasculature and subsequent migration of those cells across the endothelium into a secondary organ site. To study this process further, we analyzed transendothelial migration of human PC-3 prostate cancer cells in vitro. We isolated a subpopulation of cells, TEM4-18, that crossed an endothelial barrier more efficiently, but surprisingly, were less invasive than parental PC-3 cells in other contexts in vitro. Importantly, TEM4-18 cells were more aggressive than PC-3 cells in a murine metastatic colonization model. Microarray and FACS analysis of these cells showed that the expression of many genes previously associated with leukocyte trafficking and cancer cell extravasation were either unchanged or down-regulated. TEM4-18 cells exhibited characteristic molecular markers of an epithelial-to-mesenchymal transition (EMT), including frank loss of E-cadherin expression and upregulation of the E-cadherin repressor ZEB1. Silencing ZEB1 in TEM4-18 cells resulted in increased E-cadherin and reduced transendothelial migration. TEM4-18 cells also express N-cadherin, which was found to be necessary, but not sufficient for increased transendothelial migration. Our results extend the role of EMT in metastasis to transendothelial migration and implicate ZEB1 and N-cadherin in this process in prostate cancer cells.
2009-01-15 | GSE14405 | GEO
Project description:The naphthalene diimide compound QN-302, designed to bind to G-quadruplex DNA sequences within the promoter regions of cancer-related genes, has high anti-proliferative activity in pancreatic cancer cell lines and anti-tumor activity in several experimental models for the disease. We show here that QN-302 also causes down-regulation of the expression of the S100P gene and the S100P protein in cells and in vivo. This protein is well-established as being involved in key proliferation and motility pathways in several human cancers and has been identified as a potential biomarker in pancreatic cancer. The S100P gene contains 60 putative quadruplex-forming sequences, one of which is in the promoter region, 48 nucleotides up-stream from the transcription start site. We report biophysical and molecular modeling studies showing that this sequence forms a highly stable G-quadruplex in vitro, which is further stabilized by QN-302. We also report transcriptome analyses showing that S100P expression is highly upregulated in tissues from human pancreatic cancer tumors, compared to normal pancreas material. The extent of up-regulation is dependent on the degree of differentiation of tumor cells, with the most poorly differentiated, from more advanced disease, having the highest level of S100P expression. The experimental drug QN-302 is currently in pre-IND development (as of Q1 2023) and its ability to down-regulate S100P protein expression supports a role for this protein as a marker of therapeutic response in pancreatic cancer. These results are also consistent with the hypothesis that the S100P promoter G-quadruplex is a potential therapeutic target in pancreatic cancer at the transcriptional level for QN-302.
2023-04-01 | GSE226307 | GEO