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 both in vitro and in vivo migration of human PC-3 prostate cancer cells . We isolated 6 subpopulation of cells: TEM4-18 were isolated from in vitro transendothelial migration of PC-3 cells; GS672.Ug, GS683.LALN and JD1203.Lu are single passaged in vivo cell lines from TEM4-18; GS689.Li and GS694.LAd are twice passaged in vivo cell lines from PC-3 cells. All the subpopulations crossed an endothelial barrier more efficiently and more aggressive in a murine metastatic colonization model than parental PC-3 cells. 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. These cells exhibited characteristic molecular markers of an epithelial-to-mesenchymal transition, including frank loss of E-cadherin expression and upregulation of the E-cadherin repressor ZEB1.
Transcriptome-wide landscape of pre-mRNA alternative splicing associated with metastatic colonization.
Cell line
View SamplesThe effect of cyclic mecanical stretch on cardiac gene expression was studied in neonatal rat ventricular myocytes (NRVMs).
Mechanical stretch induced transcriptomic profiles in cardiac myocytes.
Treatment
View SamplesThe rhesus embryonic stem cell line 366.4 differentiates into serotonin neurons. RNA was extracted from ESC colonies, embryoid body (Ebs), Neurospheres in selection (N1), Proliferating serotonin neurons (N2) and differentiating serotonin neurons (N3). RNA was labeled with Enzo biotin labelling kit and hybridized to Rhesus chip from Affymetrix.
Expression profile of differentiating serotonin neurons derived from rhesus embryonic stem cells and comparison to adult serotonin neurons.
Cell line
View SamplesThe aim of this study was to determine how gene expression is changed after arsenite-induced malignant transformation of prostate epithelial cells.
Coordinate H3K9 and DNA methylation silencing of ZNFs in toxicant-induced malignant transformation.
Specimen part, Cell line, Treatment
View SamplesInhibition of miR-361-3p by locked nucleic acid (LNA)/DNA antisense oligonucleotide markedly suppressed the growth of GFP-SAS cells.
MicroRNA-361-3p is a potent therapeutic target for oral squamous cell carcinoma.
Specimen part, Cell line
View SamplesCD4+ T lymphocytes are key to immunological memory, but little is known about the lifestyle of memory CD4+ T lymphocytes. We showed that in the memory phase of specific immune responses to antigens, most of the memory CD4+ T lymphocytes relocated into the bone marrow (BM) within 3-8 weeks after their generation, a process involving integrin a2. Antigen-specific memory CD4+ T lymphocytes expressed Ly-6C to a high degree, unlike most splenic CD44hiCD62L- CD4+ T lymphocytes. In adult mice, more than 80% of Ly-6Chi CD44hiCD62L- memory CD4+ T lymphocytes were in the BM. In the BM, they are located next to IL-7-expressing VCAM-1+ stroma cells, and were in a resting state. Upon challenge with antigen, they rapidly expressed cytokines and CD154 and induced the production of high-affinity antibodies, indicating their functional activity in vivo and marking them as professional memory T helper cells
Professional memory CD4+ T lymphocytes preferentially reside and rest in the bone marrow.
Specimen part
View SamplesTo identify novel Peroxisome Proliferator-Activated Receptor gamma (PPARg) responsive secretory and/or transmembrane genes that is related to obesity, we integrated the expression data from the adipose tissue derived from obese mice with the other two data sets: expression profiling of adipocyte differentiation using ST2 cells and siRNA-mediated knockdown of Pparg during ST2 cell adipogenesis.
Fam57b (family with sequence similarity 57, member B), a novel peroxisome proliferator-activated receptor γ target gene that regulates adipogenesis through ceramide synthesis.
Specimen part
View SamplesWe used microarrays to detail transcriptional changes in the rat heart in response to doxorubicin, a chemotherapeutic drug known to induce cardiac disfunction/heart failure
Early effects of doxorubicin in perfused heart: transcriptional profiling reveals inhibition of cellular stress response genes.
No sample metadata fields
View SamplesHormones and growth factors accelerate cell proliferation of breast cancer cells, and these molecules are well investigated targets for drug development and application. The mechanisms of cell proliferation of breast cancers lacking estrogen receptor (ER) and HER2 have not been fully understood. The purpose of the present study is to find genes that are differentially expressed in breast cancers and that might significantly contribute to cell proliferation in these cancers. Forty tumor samples, consisting of ten each of immunohistochemically ER(+)/HER2(-), ER(+)/HER2(+), ER(-)/HER2(+), and ER(-)/HER2(-) cancer were analyzed using oligonucleotide microarrays. Both genes and tumor samples were subjected to hierarchical clustering. ER(+)/HER2(-) breast cancers and ER(-)/HER2(-) cancers tended to form a tumor cluster, but HER2 positive breast cancers were split into different tumor clusters.
Overexpression of E2F-5 correlates with a pathological basal phenotype and a worse clinical outcome.
No sample metadata fields
View SampleseIF4E, the major cap-binding protein, has long been considered limiting for translating the mammalian genome. However, the requirement for eIF4E dose at an organismal level remains unexplored. By generating an Eif4e haploinsufficient mouse, we surprisingly found that 50% reduction in eIF4E, while compatible with normal development and global protein synthesis, significantly impeded cellular transformation and tumorigenesis. Genome-wide translational profiling uncovered a translational program induced by oncogenic transformation and revealed a critical role for eIF4E dose specifically in translating a network of mRNAs enriched for a unique 5UTR signature. In particular, we demonstrate that eIF4E dose is essential for translating mRNAs regulating reactive oxygen species (ROS) that fuel transformation and cancer cell survival in vivo. Therefore, mammalian cells have evolved surplus eIF4E levels that cancer cells hijack to drive a translational program supporting tumorigenesis
Differential Requirements for eIF4E Dose in Normal Development and Cancer.
Specimen part
View Samples