Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

In vivo transcriptome profiling of control and GANAB-KD UMUC3 bladder carcinoma cells [scRNA-Seq]

ABSTRACT: Carcinoma cells achieve malignant progression and therapy resistance through de-differentiation. While differentiation therapy has proven to be highly efficient in acute promyelocytic leukemia, this therapeutic strategy has not been successfully applied in human solid tumors. Here, we identify α-Glucosidase II (GANAB) as a novel driver of bladder cancer de-differentiation using a systemic biology approach and demonstrate its potential to serve as a therapeutic target of solid tumor differentiation therapy. Partial knock-out of GANAB by CRISPR Cas9 differentiates one of the most aggressive bladder carcinoma line into a non-invasive papillary form in vivo and decreases chemotherapy resistance in vitro. As differentiation and de-differentiation program are mostly activated in vivo, we labelled control and GANAB-KD cells with a lentivirus to express a H2B-EGFP localized in the nuclei. After sorting by BD FACS Aria II, cells were lyzed for RNA-sequencing.

ORGANISM(S): Homo sapiens

PROVIDER: GSE164041 | GEO | 2020/12/31

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

In vivo transcriptome profiling of control and GANAB-KD UMUC3 bladder carcinoma cells [bulk]

Project description:Carcinoma cells achieve malignant progression and therapy resistance through de-differentiation. While differentiation therapy has proven to be highly efficient in acute promyelocytic leukemia, this therapeutic strategy has not been successfully applied in human solid tumors. Here, we identify α-Glucosidase II (GANAB) as a novel driver of bladder cancer de-differentiation using a systemic biology approach and demonstrate its potential to serve as a therapeutic target of solid tumor differentiation therapy. Partial knock-out of GANAB by CRISPR Cas9 differentiates one of the most aggressive bladder carcinoma line into a non-invasive papillary form in vivo and decreases chemotherapy resistance in vitro. As differentiation and de-differentiation program are mostly activated in vivo, we labelled control and GANAB-KD cells with a lentivirus to express a H2B-EGFP localized in the nuclei. After sorting by BD FACS Aria II, cells were lyzed for RNA-sequencing.

2020-12-31 | GSE164042 | GEO

Expression data from UMUC3 cells transduced with non-targeted shRNA and shRNA specific to AGL

Project description:Loss of Amylo-alpha-1-6-glucosidase-4-alpha-glucanotransferase (AGL) drives bladder cancer growth. Low AGL expression predicts poor patient outcome. Currently no specific therapeutically tractable targets/pathways exist that could be used to treat patients with low AGL expressing bladder tumors. To address this issue we carried out a transcriptome analysis in human bladder cancer cells with and without AGL expression to identify pro-tumorigenic pathways upregulated with AGL loss. We identified and validated that hyaluronic acid (HA) synthase 2 (HAS2) expression and subsequent HA synthesis is upregulated with AGL loss. We validated that HAS2 and consequent HA synthesis drive tumor growth and that genetic and pharmacologic inhibition of these respectively is a viable therapeutic option in xenograft models. We further established that bladder cancer patients with low AGL expression and high HAS2 expression have poor outcome. Together, this data provide preclinical evidence for personalized targeting of HAS2/HA signaling in patients with low AGL expressing tumors.

2015-09-26 | GSE73456 | GEO

RNA-Seq of circHIPK3 knockdown (KD) samples in UMUC3 and J82

Project description:We profile gene expression upon circHIPK3 KD in two bladder cancer cell lines UMUC3 and J82

2021-10-01 | GSE148824 | GEO

RNA-Seq of circCDYL knockdown (KD) samples in HepG2, J82, and UMUC3 cells and of GRWD1, IGF2BP1, and IGF2BP2 knockdown (KD) samples in J82 and UMUC3 cells

Project description:We profile gene expression upon circCDYL KD in HepG2 cells and in two bladder cancer cell lines J82 and UMUC3 as well as upon knockdown of the RNA binding proteins (RBP) GRWD1, IGF2BP1, and IGF2BP2 in J82 and UMUC3

2020-11-11 | GSE146726 | GEO

In vivo transcriptome profiling of control and GANAB-KD UMUC3 bladder carcinoma cells

Project description:In vivo transcriptome profiling of control and GANAB-KD UMUC3 bladder carcinoma cells

| PRJNA688703 | ENA

Biased Expression of the FOXP3Î3 Isoform in Aggressive Bladder Cancer Mediates Differentiation and Cisplatin Chemotherapy Resistance

Project description:This study shows for the first time that the FOXP3Î3 isoform is preferentially expressed in bladder cancer and induces a more aggressive and luminal isoform is preferentially expressed in bladder cancer and induces a more aggressive and luminal regulation of cancer differentiation and the plasticity amongst cancer subtypes which can be leveraged to optimize therapeutic regimens. These findings also identify a novel molecular marker as a putative companion diagnostic to guide therapy and target to undermine chemotherapy resistance. examination of RNA-Seq in two bladder cancer cell lines

2016-08-05 | E-GEOD-81157 | biostudies-arrayexpress

RNAseq in JARID2 siRNA-treated in vitro differentiated human primary adipocytes

Project description:RNAseq was performed in siJARID2 and control siRNA-treated human adipose tissue derived stem cells (hASC). The tretment of siRNA was performed by electroporation one day before induction of differentiation in vitro. The cells were lyzed and RNA was purified on day 6 (mid differentiation) and day 13 (full differentiation) from differentiation start.

2021-05-18 | GSE164413 | GEO

Expression profile of PBMCs following decitabine treatment

Project description:The epigenetic regulation, for example, DNA methylation, controls the development and differentiation of both tumor cells and immunocytes. Treatment with DNA demethylating agent (such as decitabine) has shown a dramatic clinical benefit in hematological malignancies and solid tumors. However, the influence of epigenetic therapy on host immune system remains unclear. To investigate the effects of low-dose decitabine therapy on T cells, We collected whole blood samples from two solid tumor patients pre and post low-dose decitabine therapy, and detected the expression profiles of PBMCs.

2016-06-30 | E-GEOD-72686 | biostudies-arrayexpress

Skeletal muscle gene expression in the wild type and the GAA knock-out mice, a model of Pompe disease

Project description:Pompe disease is a Lysosomal glycogen storage disorder due to the deficiency of acid alpha glucosidase. The enzyme degrades glycogen to glucose and its deficiency results in progressive enlargement of glycogen-filled lysosomes in multiple tissues with skeletal and cardiac muscle most severely affected clinically. Clinical spectrum ranges from most severe infantile cardiomegally and skeletal muscle myopathy to milder late onset forms with only skeletal muscle pathology. The currently available enzyme replacement therapy has only limited effect in skeletal muscle. Here we use RNA sequencing of therapy-resistant skeletal muscle (white part of gastrocnemius muscle) to identify the differencies between the diseased and healthy muscle. Total RNA was obtained from gastrocnemius muscle (white part) of acid alpha glucosidase knock-out and wild-type mice.

2017-05-13 | E-GEOD-57980 | biostudies-arrayexpress

Niacin restriction with NAMPT-inhibition is synthetic lethal to neuroendocrine carcinoma (Mouse NAMPT targeted therapy)

Project description:NAMPT plays a major role in NAD biosynthesis in many cancers and is an attractive potential cancer target. However, factors dictating therapeutic efficacy of NAMPT inhibitors (NAMPTi) are unclear. We report that neuroendocrine phenotypes predict lung and prostate carcinoma vulnerability to NAMPTi, and that NAMPTi therapy against those cancers is enhanced by dietary modification. Neuroendocrine differentiation of tumor cells was associated with down-regulation of genes relevant to QPRT-dependent de novo NAD synthesis, promoting NAMPTi susceptibility in vitro. We also found that circulating nicotinic acid riboside (NAR), a non-canonical niacin absent in culture media, antagonizes NAMPTi efficacy as it fuels NAMPT-independent but NMRK1-dependent NAD synthesis in tumors. In mouse transplantation models, depleting blood NAR by nutritional or genetic manipulations was synthetic lethal to tumors when combined with NAMPTi. Our findings provide a rationale for simultaneous targeting of NAR metabolism and NAMPT therapeutically in neuroendocrine carcinoma. Mouse NAMPT targeted therapy is reported in the current study <a href='https://www.ebi.ac.uk/metabolights/MTBLS7252' rel='noopener noreferrer' target='_blank'>MTBLS7252</a>.Cell NAMPTi treatment is reported in <a href='https://www.ebi.ac.uk/metabolights/MTBLS7251' rel='noopener noreferrer' target='_blank'>MTBLS7251</a>.Mouse NAD targeted time-course is reported in <a href='https://www.ebi.ac.uk/metabolights/MTBLS7253' rel='noopener noreferrer' target='_blank'>MTBLS7253</a>.

2023-10-10 | MTBLS7252 | MetaboLights

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