We have sequenced the polysome-associated translating mRNAs from stage-matched wild-type and eif3ha morphant embryos at ~24 hpf stage to identify transcripts translationally regulated by eIF3ha. As a control, we have also sequenced total mRNAs from the stage-matched wild-type and eif3ha morphants as well at ~ 24 hpf. Overall design: Polysome-associated mRNAs were isolated from 300 zebrafish embryos. Total RNA was isolated from 50 zebrafish embryos. Single 36-base pair reads were sequenced on the Illumina Genome Analyzer Iix.
Translation initiation factor eIF3h targets specific transcripts to polysomes during embryogenesis.
No sample metadata fields
View SamplesRNA sequencing of nucleus pulposus cells transduced with shRNA (control or TonEBP-targeted) and either untreated or treated with TNF-a (24h) Overall design: Total mRNA was collected from primary nucleus pulposus cells and subjected to RNA sequencing, n=3 for all experimental groups
TNF-α promotes nuclear enrichment of the transcription factor TonEBP/NFAT5 to selectively control inflammatory but not osmoregulatory responses in nucleus pulposus cells.
No sample metadata fields
View SamplesUlcerative colitis (UC) and Crohns disease (CD) are inflammatory bowel diseases (IBD) with variable, overlapping clinical features and complex pathophysiologies. To identify pathogenic processes underlying these disease subtypes, using single endoscopic pinch biopsies to estabolish 36 expression profiles, we elucidated gene expression patterns of active and inactive areas of UC and CD, and compared these to infectious colitis and healthy controls.
Genome-wide gene expression differences in Crohn's disease and ulcerative colitis from endoscopic pinch biopsies: insights into distinctive pathogenesis.
No sample metadata fields
View SamplesPancreatic ductal adenocarcinoma (PDAC) is a nearly uniformly lethal malignancy, with most patients facing an adverse clinical outcome. Given the pivotal role of aberrant Notch signaling in the initiation and progression of PDAC, we investigated the effect of MRK-003, a potent and selective -secretase inhibitor, in preclinical PDAC models. We used a panel of human PDAC cell lines, as well as patient-derived PDAC xenografts, to determine whether pharmacological targeting of the Notch pathway could inhibit pancreatic tumor growth and potentiate gemcitabine sensitivity. In vitro, MRK-003 treatment downregulated the canonical Notch target gene Hes-1, significantly inhibited anchorage independent growth, and reduced the subset of CD44+CD24+ and aldehyde dehydrogenase (ALDH)+ cells that have been attributed with tumor initiating capacity. Ex vivo pretreatment of PDAC cells with MRK-003 in culture significantly inhibited the subsequent engraftment in immunocompromised mice. In vivo, MRK-003 monotherapy significantly blocked tumor growth in 5 of 9 (56%) patient-derived PDAC xenografts. Moreover, a combination of MRK-003 and gemcitabine showed enhanced antitumor effects compared to gemcitabine alone in 4 of 9 (44%) PDAC xenografts. Baseline gene expression analysis of the treated xenografts indicated that upregulation of nuclear factor kappa B (NFB) pathway components was associated with the sensitivity to single MRK-003, while upregulation in B-cell receptor (BCR) signaling and nuclear factor erythroid-derived 2-like 2 (NRF2) pathway correlated with response to the combination of MRK-003 with gemcitabine. The preclinical findings presented here provide further rationale for small molecule inhibition of Notch signaling as a therapeutic strategy in PDAC.
The gamma secretase inhibitor MRK-003 attenuates pancreatic cancer growth in preclinical models.
Specimen part
View SamplesIn order to identify biologically relevant tumor markers with prognostic significance, we set out to analyze gene expression profiling of tumor and adjacent non-tumor tissues from PDAC cases.
DPEP1 inhibits tumor cell invasiveness, enhances chemosensitivity and predicts clinical outcome in pancreatic ductal adenocarcinoma.
Specimen part
View SamplesIn order to examine the consequences of human miR-34a induction on the transcriptome, HCT116 cells (a colon cancer cell line) were infected with a retrovirus that produces miR-34a. Gene expression profiles were then monitored using Affymetrix microarrays.
Transactivation of miR-34a by p53 broadly influences gene expression and promotes apoptosis.
No sample metadata fields
View SamplesTumors from pancreatic cancer specimens obtained at surgery were used for efficacy testing and biologic analysis
Coordinated epidermal growth factor receptor pathway gene overexpression predicts epidermal growth factor receptor inhibitor sensitivity in pancreatic cancer.
No sample metadata fields
View SamplesIn this study Panc-1 cells and BxPC-3 cells were cultured. The cells were harvested (untreated control 'cont') for RNA extraction, or treated for 3 hours with various exosomes preparations. The exosomes were collected from BJ human foreskin fibroblast culture supernatant without further processing (control exosomes or 'CE'), or engineered to contain scrambled siRNA ('scr') or KRASG12D siRNA ('iExo). Two or three distinct wells of cells were evaluated per treatment condition and assigned a well number (well -1, -2 or 3).
Generation and testing of clinical-grade exosomes for pancreatic cancer.
Cell line, Treatment
View SamplesTranscriptome analysis was performed from human U87 glioblastoma cell clones: U87 IRE1.NCK DN (U87dn, IRE1 dominant negative) and U87 control (U87ctrl, empty plasmid). Cells were grown in DMEM supplemented with 10% FBS and glutamine for 16 hours in culture prior mRNA isolation and analyses
Inositol-requiring enzyme 1alpha is a key regulator of angiogenesis and invasion in malignant glioma.
Cell line
View SamplesComparison of malic enzyme 3 (ME3) depleted vs non-depleted xenograft tumors. ME3 is an isoform of ME2. Overall design: Sub-cutaneous tumors of nude mice injected with PATU-ishME3 (shRNA against ME3) and treated +/- Dox to knockdown ME3. 4 tumors off-dox and 2 tumors on-dox
Genomic deletion of malic enzyme 2 confers collateral lethality in pancreatic cancer.
Specimen part, Cell line, Subject
View Samples