Browse
Submit Data
Databases
API
Help

Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

33 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

M12-8: MRX34 Biomarker study in animals bearing Hep3B orthotopic liver tumors [Illumina]

ABSTRACT: To identify direct tumor mRNA targets of miR-34a, tumor RNAs isolated from whole tumors from animals treated with negative control and MRX34 Hep3B cells were surgically implanted into the livers of Nod/Scid mice and allow to grow for multiple weeks. Once serum AFP levels reached levels consistent with tumor growth of ~80-100 mg, animals were subjected to a single IV injection of MRX34. Twenty-four hours later animals were sacrificed, tumors resected and RNA isolated for subsequent microarray analysis.

ORGANISM(S): Homo sapiens

SUBMITTER: Christopher Daige

PROVIDER: E-GEOD-58892 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

ACCESS DATA

Json Xml

Publications

Systemic delivery of a miR34a mimic as a potential therapeutic for liver cancer.

Daige Christopher L CL Wiggins Jason F JF Priddy Leslie L Nelligan-Davis Terri T Zhao Jane J Brown David D

Molecular cancer therapeutics 20140722 10

miR34a is a tumor-suppressor miRNA that functions within the p53 pathway to regulate cell-cycle progression and apoptosis. With apparent roles in metastasis and cancer stem cell development, miR34a provides an interesting opportunity for therapeutic development. A mimic of miR34a was complexed with an amphoteric liposomal formulation and tested in two different orthotopic models of liver cancer. Systemic dosing of the formulated miR34a mimic increased the levels of miR34a in tumors by approximat ...[more]

PMID: 25053820

Similar Datasets

M12-28: MRX34 Biomarker study in animals bearing HuH7 orthotopic liver tumors [Affymetrix]

Project description:To identify direct tumor mRNA targets of miR-34a, tumor RNAs isolated from whole tumors from animals treated with negative control and MRX34 HuH7 cells were surgically implanted into the livers of Nod/Scid mice and allow to grow for multiple weeks. Once serum AFP levels reached levels consistent with tumor growth of ~80-100 mg, animals were subjected to a single IV injection of MRX34. Twenty-four hours later animals were sacrificed, tumors resected and RNA isolated for subsequent microarray analysis.

2014-11-05 | E-GEOD-58800 | biostudies-arrayexpress

MRX34 Biomarker study in animals bearing Hep3B orthotopic liver tumors

Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

2014-11-05 | E-GEOD-58893 | biostudies-arrayexpress

M12-8: MRX34 Biomarker study in animals bearing Hep3B orthotopic liver tumors [Illumina]

Project description:To identify direct tumor mRNA targets of miR-34a, tumor RNAs isolated from whole tumors from animals treated with negative control and MRX34

2014-11-05 | GSE58892 | GEO

M12-28: MRX34 Biomarker study in animals bearing HuH7 orthotopic liver tumors [Affymetrix]

Project description:To identify direct tumor mRNA targets of miR-34a, tumor RNAs isolated from whole tumors from animals treated with negative control and MRX34

2014-11-05 | GSE58800 | GEO

Gene expression profiling of metastatic lung cancer cell lines

Project description:During malignant disease progression, the extracellular matrix (ECM) of epithelial tumors accumulates inter-molecular cross-links between collagen strands; these cross-links enhance ECM stiffness and trigger tumor cell invasion and dissemination, but the mechanisms that regulate intra-tumoral collagen maturation have not been fully defined. Using a new mouse model of metastatic lung adenocarcinoma driven by mutant K-ras expression and Cdkn1a inactivation, we showed that tumor cell invasion and metastasis are driven by high expression of lysyl hydroxylase 2 (LH2), an enzyme that hydroxylates telomeric lysine (Lys) residues on collagen. We interbred KrasLA1 mice, which develop non-metastatic lung adenocarcinomas at 8-10 months of age because of the expression of a somatically activated K-rasG12D allele, with Cdkn1a-/- mice, which develop sarcomas and B cell lymphomas because of depletion of p21. Cohorts were generated that had neither, either, or both mutant alleles. KrasLA1 mice that were p21-deficient (KC mice) had a shorter mean time to death than did p21-replete ones. We established cell lines from the tumors, and compared cell lines from highly metastatic tumors with those from poorly metastatic tumors.

2015-03-12 | E-GEOD-49315 | biostudies-arrayexpress

Intact N-glycopeptides and proteomics from HCC tissue tumors with low and high AFP concentrations

Project description:Hepatocellular carcinoma (HCC) is still one of the malignant tumors with high morbidity and mortality in China and worldwide. Although AFP have been widely used as important biomarkers for HCC diagnosis and evaluation, the AFP level has a huge variation among HCC patient populations. Understanding the intrinsic heterogeneities of HCC associated with AFP levels is essential for the molecular mechanism studies of HCC with different AFP levels as well as for the potential early diagnosis and personalized treatment of HCC with AFP negative. Here, an integrated glycoproteomic and proteomic analysis of low and high AFP level of HCC tumors was performed to investigate the intrinsic heterogeneities of site-specific glycosylation associated with different AFP levels of HCC. we identified many commonly altered site-specific glycans from HCC tumors regardless of AFP levels, including decreased modifications by oligo-mannose and sialylated bi-antennary glycans, and increased modifications by bisecting glycans. By relative quantifying the intact glycopeptides between low and high AFP tumor groups, the great heterogeneities of site-specific N-glycans between two groups of HCC tumors were also uncovered. We found that several sialylated but not core fucosylated tri-antennary glycans were uniquely high-regulated in low AFP level of HCC tumors, while many core fucosylated bi-antennary or hybrid glycans as well as bisecting glycans were uniquely increased in high AFP tumors. The data provide a valuable resource for future HCC studies regarding the mechanism, heterogeneities and new biomarker discovery.

2020-03-19 | PXD016406 | Pride

siRNA Administration Against AFP Inhibits Hepatocellular Carcinoma Proliferation in Vitro and Progression in Mice

Project description:Increased α-fetoprotein (AFP) levels have been reported to predict a poor prognosis in hepatocellular carcinoma (HCC). We assessed the mechanism of AFP involvement in the progression of HCC and determined whether AFP could be a molecular target. We used human HCC cell lines to assess proliferation and apoptosis response to exogenous AFP. We introduced AFP small interfering RNA (siRNA) into HCC cell lines to examine whether it could inhibit cell proliferation and anti-apoptotic properties. The effects of systemically introduced AFP siRNA were assessed using a tumor xenotransplantation model. The effects of AFP on gene expression in HCC cell lines and human HCC specimens were examined. Exogenous AFP induced cell proliferation dose-dependently and inhibited apoptosis induced by 5-fluorouracil (5-FU) in all cell lines examined. AFP siRNA inhibited the proliferation of AFP-producing HCC cell lines and induced apoptosis in co-cultures with 5-FU. Tumor sizes in mice treated with AFP siRNA were significantly smaller than those in controls. AFP siRNA administration in mice induced a low proliferation index and a high apoptosis index in tumors. cDNA microarray analysis, reverse transcription-polymerase chain reaction (RT-PCR), and Western blot using HepG2 and HLE cells with AFP showed that AFP reduced expression of genes related to apoptosis (DFFB) and tumor suppression (NDRG2). Expression of these molecules was also suppressed in human HCC tissues that overexpress AFP. AFP is not only a passive tumor marker, but also an active tumor stimulator through several mechanisms. AFP siRNA introduction may be of possible therapeutic use for HCC. Keywords: Genetic modification

2008-12-31 | GSE12307 | GEO

siRNA Administration Against AFP Inhibits Hepatocellular Carcinoma Proliferation in Vitro and Progression in Mice

Project description:Increased ?-fetoprotein (AFP) levels have been reported to predict a poor prognosis in hepatocellular carcinoma (HCC). We assessed the mechanism of AFP involvement in the progression of HCC and determined whether AFP could be a molecular target. We used human HCC cell lines to assess proliferation and apoptosis response to exogenous AFP. We introduced AFP small interfering RNA (siRNA) into HCC cell lines to examine whether it could inhibit cell proliferation and anti-apoptotic properties. The effects of systemically introduced AFP siRNA were assessed using a tumor xenotransplantation model. The effects of AFP on gene expression in HCC cell lines and human HCC specimens were examined. Exogenous AFP induced cell proliferation dose-dependently and inhibited apoptosis induced by 5-fluorouracil (5-FU) in all cell lines examined. AFP siRNA inhibited the proliferation of AFP-producing HCC cell lines and induced apoptosis in co-cultures with 5-FU. Tumor sizes in mice treated with AFP siRNA were significantly smaller than those in controls. AFP siRNA administration in mice induced a low proliferation index and a high apoptosis index in tumors. cDNA microarray analysis, reverse transcription-polymerase chain reaction (RT-PCR), and Western blot using HepG2 and HLE cells with AFP showed that AFP reduced expression of genes related to apoptosis (DFFB) and tumor suppression (NDRG2). Expression of these molecules was also suppressed in human HCC tissues that overexpress AFP. AFP is not only a passive tumor marker, but also an active tumor stimulator through several mechanisms. AFP siRNA introduction may be of possible therapeutic use for HCC. Keywords: Genetic modification Two-condition experiment, Control vs. AFP-stimulated cells.

2008-12-30 | E-GEOD-12307 | biostudies-arrayexpress

RNA-seq of Sting overexpressing orthotopic pancreas tumors

Project description:Murine pancreatic PKCY tumor cells (p53fl/+;KrasLSL-G12D/+;Pdx1-Cre;Rosa26LSL-YFP) were engineered to overexpress Sting or empty vector control. Tumor cells were orthotopically transplanted into the pancreas of syngeneic littermates. Tumors were harvested and RNA seq for transcriptomic differences was performed.

2021-09-06 | E-MTAB-10722 | biostudies-arrayexpress

Regulation of dendritic cell genes by alpha fetoprotein

Project description:Human dendritic cells (DC) are suppressed by tumor-derived alpha fetoprotein (AFP), but less so by cord blood-derived normal AFP. We tested human DC from 5 healthy donors for transcriptional changes induced by tumor (tAFP) or cord blood (nAFP) AFP, vs. chicken ovalbumin (OVA) control.

2014-12-23 | E-GEOD-62005 | biostudies-arrayexpress

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data