COLO 320 (Human colorectal cancer cell line) xenograft: Control (Xenograft without rat mesenchymal stem cells (MSCs)) vs Xenograft with rat MSCs
ABSTRACT: Transcriptional profiling of COLO 320 xenograft tumor cells comparing control COLO 320 xenograft without co-implanted rat MSCs with COLO 320 xenograft with co-implanted rat MSCs. The latter makes co-implanted MSCs visualization possible by using MSCs labeled by GFP under FACS and single cell microscopy. Two-condition experiment, COLO 320 xenograft without rat MSCs [COLO320 MSC(-)] vs. COLO 320 xenograft with rat MSCs [COLO320 MSC(+)]. Biological replicates: 1 control, 1 sample, paired xengraft tumor cells grown and harvested from the same mouse host. One replicate per array.
Project description:Wnt/β-catenin signaling is activated in colorectal cancer (CRC) and is involved in CRC growth. Tankyrase, a poly(ADP-ribose) polymerase family member, destabilizes Axin and positively regulates the Wnt/β-catenin signaling. Tankyrase inhibitors efficiently suppress CRC cell proliferation. We established 320-IWR cells, which showed resistance to tankyrase inhibitor IWR-1, from human CRC COLO-320DM cells. We analyzed gene expression profile of 320-IWR cells (320IWR_1,_2) and parental COLO-320DM cells (COLO320_1,_2). Overall design: We continuously treated COLO-320DM cells with a tankyrase inhibitor IWR-1 and established a tankyrase inhibitor-resistant cell line, 320-IWR. We compared gene expression between COLO-320DM (COLO320_1,_2) and 320-IWR (320IWR_1,_2) cells.
Project description:This SuperSeries is composed of the following subset Series: GSE38814: Glioblastoma Orthotopic Xenograft Transcriptome GSE38815: Glioblastoma Xenograft Comparative Genomic Hybridization Arrays Refer to individual Series
Project description:RNAseq is performed (50bp single end reads) on SW480, HT-29, HCT-15, HCT-116, COLO 205, and COLO 320 cell lines after DMSO or JQ1 treatment Overall design: Examination of transcriptomic changes after JQ1 treatment
Project description:Background: Bronchopulmonary dysplasia (BPD), the most common complication of extreme preterm birth, can be caused by oxygen-related lung injury and is characterized by impaired alveolar and vascular development. Mesenchymal stromal cells (MSCs) have lung protective effects. Conversely, BPD is associated with increased MSCs in tracheal aspirates. Objective: To determine whether endogenous lung (L-)MSCs are perturbed in a well-established oxygen-induced rat model mimicking BPD features. Methods: Rat pups were exposed to room air or 95% oxygen from birth to postnatal day 10. On day 12, CD146+ L-MSCs were isolated and characterized according to the International Society for Cellular Therapy criteria. Epithelial and vascular repair potential were tested by scratch assay and endothelial network formation respectively, immune function by mixed lymphocyte reaction assay. Microarray analysis was performed using the Affymetrix GeneChip and gene set enrichment analysis (GSEA) software. Results: CD146+ L-MSCs isolated from rat pups exposed to hyperoxia had decreased CD73 expression and inhibited lung endothelial network formation. CD146+ L-MSCs indiscriminately promoted epithelial wound healing and limited T-cell proliferation. Expression of potent anti-angiogenic genes of the axonal guidance cue and CDC42 pathways was increased after in vivo hyperoxia, whereas genes of the anti-inflammatory JAK/STAT and lung/vascular growth promoting Fibroblast Growth Factor (FGF) pathways were decreased. Conclusions: In vivo hyperoxia exposure alters the pro-angiogenic effects and FGF expression of L-MSCs. Additionally, decreased CD73 and JAK/STAT expression suggest decreased immune function. L-MSC function may be perturbed and contribute to BPD pathogenesis. These findings may lead to improvements in manufacturing exogenous MSCs with superior repair capabilities. Overall design: For the microarray analysis, CD146+ L-MSCs (passage 2) were expanded in 5% O2 (physiological oxygen) culture conditions and collected for RNA isolation. The experiment consisted of two groups: L-MSCs isolated from P12 rat pups exposed to 95% O2 from P0 to P10 (n=3) and L-MSCs isolated from P12 room air control pups (n=3).
Project description:To investigate the altered patways among sarcomas and MSCs, gene expression profiles were comared among rat osteosarcoma and malignant histiocytoma (MFH) to mesenchymal stem cells (MSCs) from syngeneic origin. Several altered pathways have identified including down-regulation of Wnt, Cell adhesion, ECM interaction and up-regulation of Hedgehog, cell cycling pathways in rat sarcomas compared to MSCs. Gene expression array analysis was perfromed for the samples of rat osteosarcoma COS1NR and malignant fibrous histiocytoma MFH1NR cell lines, bothe established from chemically induced tumors in F344 rats by 4-HAQO, and rat mesenchymal stem cells freshly isolated from femur bone marrow of F344 rats.
Project description:To investigate the altered patways among sarcomas and MSCs, gene expression profiles were comared among rat osteosarcoma and malignant histiocytoma (MFH) to mesenchymal stem cells (MSCs) from syngeneic origin. Several altered pathways have identified including down-regulation of Wnt, Cell adhesion, ECM interaction and up-regulation of Hedgehog, cell cycling pathways in rat sarcomas compared to MSCs. Overall design: Gene expression array analysis was perfromed for the samples of rat osteosarcoma COS1NR and malignant fibrous histiocytoma MFH1NR cell lines, bothe established from chemically induced tumors in F344 rats by 4-HAQO, and rat mesenchymal stem cells freshly isolated from femur bone marrow of F344 rats.
Project description:Comparison of expression profiles in adipose derived MSCs (AD-MSCs) without or with transfection of siR-EID1 and shR-EID1 and cord blood-derived HSCs (CB-HSCs). After MSCs were transfected with sRNA-EID1, they could be converted into HSCs. The goal was to determine possible molecular mechanisms of MSC transdetermination. Two-condition experiments: AD-MSCs vs CB-HSCs, and AD-MSCs transfected with the combination of siR-EID1 and shR-EID1 vs AD-MSCs transfected with shR-EID1.
Project description:The number of relevant and well-characterized cell lines and xenograft models for studying human breast cancer are few, and may represent a limitation for this field of research. With the aim of developing new breast cancer model systems for in vivo studies of hormone dependent and independent tumor growth, progression and invasion, and for in vivo experimental therapy studies, we collected primary mammary tumor specimens from patients, and implanted them in immunodeficient mice. Primary tumor tissue from 29 patients with breast cancer was implanted subcutaneously with matrigel in SCID mice, in the presence of continuous release of estradiol. The tumors were transferred into new animals when reaching a diameter of 15mm and engrafted tumors were harvested for morphological and molecular characterization from passage six. Further, gene expression profiling was performed using Agilent Human Whole Genome Oligo Microarrays, as well as DNA copy number analysis using Agilent Human Genome CGH 244K Microarrays. Of the 30 primary tumors implanted into mice (including two implants from the same patient), two gave rise to viable tumors beyond passage ten. One showed high expression levels of estrogen receptor-alpha protein (ER) while the other was negative. Histopathological evaluation of xenograft tumors was carried out at passage 10-12; both xenografts maintained the morphological characteristics of the original tumors (classified as invasive grade III ductal carcinomas). The genomic profile of the ER-positive xenograft tumor resembled the profile of the primary tumor, while the profile obtained from the ER-negative parental tumor was different from the xenograft. However, the ER-negative parental tumor and xenograft clustered on the same branch using unsupervised hierarchical clustering analysis on RNA microarray expression data of "intrinsic genes". A significant variation was observed in the expression of extracellular matrix (ECM)-related genes, which were found downregulated in the engrafted tumors compared to the primary tumor. By IHC and qRT-PCR we found that the downregulation of stroma-related genes was compensated by the overexpression of such molecules by the mouse host tissue. The two established breast cancer xenograft models showed different histopathological characteristics and profound diversity in gene expression patterns that in part can be associated to their ER status and here described as basal-like and luminal-like phenotype, respectively. These two new breast cancer xenografts represent useful preclinical tools for developing and testing of new therapies and improving our knowledge on breast cancer biology. Overall design: Set of arrays organized by shared biological context, such as organism, tumors types, processes, etc.