Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Expression data from xenograft tumors derived from LoVo colon cancer lines +/- constitutive LIN28B expression

ABSTRACT: We sought to elucidate functions of LIN28B and potential mechanisms whereby it may promote metastasis by comparing the gene expression profile of LIN28B metastases to primary tumors. Accordingly, we performed microarray analysis on total RNA isolated from empty vector tumors, LIN28B-LoVo tumors, and LIN28B-LoVo metastases

ORGANISM(S): Homo sapiens

PROVIDER: GSE26335 | GEO | 2010/12/29

SECONDARY ACCESSION(S): PRJNA142245

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Shared Molecules

Only show the datasets with similarity scores above: 0.5

Threshold

0.5

Similar Datasets

Expression data from xenograft tumors derived from LoVo colon cancer lines +/- constitutive LIN28B expression

Project description:We sought to elucidate functions of LIN28B and potential mechanisms whereby it may promote metastasis by comparing the gene expression profile of LIN28B metastases to primary tumors. Accordingly, we performed microarray analysis on total RNA isolated from empty vector tumors, LIN28B-LoVo tumors, and LIN28B-LoVo metastases Constitutive LIN28B expression was achieved in the LoVo (ATCC #CCL-229) colon cancer cell line via retroviral transduction of MSCV-PIG-LIN28B. xenografts were produced via injection of 1x106 cells subcutaneously into the rear flanks of nude mice. Microarrays were conducted on primary tumors from empty vector and LIN28B-expressing cells, as well as metastases derived from primary tumors constitutively expressing LIN28B. (Note: metastases did not occur with empty vector tumors)

2010-12-29 | E-GEOD-26335 | biostudies-arrayexpress

Expression data from LoVo colon cancer lines +/- constitutive LIN28B expression

2010-12-29 | GSE26334 | GEO

Expression data from LoVo colon cancer lines +/- constitutive LIN28B expression

Project description:We sought to elucidate the molecular mechanisms whereby LIN28B functions by comparing the gene expression profile of cells constitutively expressing LIN28B to empty vector controls. Accordingly, we performed microarray analysis on total RNA isolated from empty vector LoVo and LIN28B-expressing LoVo colon cancer cell lines. Constitutive LIN28B expression was achieved in the LoVo (ATCC #CCL-229) colon cancer cell line via retroviral transduction of MSCV-PIG-LIN28B. Contol = empty vector MSCV-PIG.

2010-12-29 | E-GEOD-26334 | biostudies-arrayexpress

LIN28B and colon cancer

Project description:This SuperSeries is composed of the following subset Series: GSE26334: Expression data from LoVo colon cancer lines +/- constitutive LIN28B expression GSE26335: Expression data from xenograft tumors derived from LoVo colon cancer lines +/- constitutive LIN28B expression Refer to individual Series

2010-12-29 | E-GEOD-26336 | biostudies-arrayexpress

LIN28B promotes cell invasion and colorectal cancer metastasis via CLDN1 and NOTCH3

Project description:The RNA-binding protein LIN28B is overexpressed in over 30% of patients with colorectal cancer (CRC) and is associated with poor prognosis. In the present study, we unravel a novel mechanism by which LIN28B regulates colonic epithelial cell-cell junctions and CRC metastasis. Using human CRC cells (DLD-1, Caco-2 and LoVo) with either knockdown or overexpression of LIN28B, we identified Claudin 1 (CLDN1) tight junction protein as a direct downstream target and effector of LIN28B. RNA immunoprecipitation revealed that LIN28B directly binds to and post-transcriptionally regulates CLDN1 mRNA. Furthermore, using in vitro assays and a novel murine model of metastatic CRC, we show that LIN28B-mediated CLDN1 expression enhances collective invasion, cell migration, and metastatic liver tumor formation. Bulk RNA-sequencing of the metastatic liver tumors identified NOTCH3 as a downstream effector of the LIN28B-CLDN1 axis. Additionally, genetic and pharmacologic manipulation of NOTCH3 signaling revealed that NOTCH3 was necessary for invasion and metastatic liver tumor formation. In summary, our results suggest that LIN28B promotes invasion and liver metastasis of CRC by post-transcriptionally regulating CLDN1 and activating NOTCH3 signaling. This discovery offers a promising new therapeutic option for metastatic CRC to the liver, an area where therapeutic advancements have been relatively scarce.

2023-09-14 | GSE234513 | GEO

microRNA array of LoVo cells and LoVo-Small Extracellular Vesicles

Project description:LoVo cells were cultured in sEV-depleted (160,000xg, 16h) complete medium and the supernatant were collected after 72h. sEVs were purified and centrifuged at 100,000xg for 2.5h using a Beckman SW41Ti rotor to know the miRNA in LoVo cells and LoVo-Small Extracellular Vesicles

2019-07-01 | GSE117866 | GEO

Calu6 and LoVo xenograft mRNA expression profiles in response to cediranib treatment

Project description:Calu6 and LoVo xenograft mRNA expression profiles in response to cediranib treatment

2013-09-09 | E-MTAB-1627 | biostudies-arrayexpress

Lin28b promotes fetal B lymphopoiesis through the transcription factor Arid3a [Lin28b & Let7 transduction]

Project description:Mouse B cell precursors from fetal liver and adult bone marrow generate distinctive B cell progeny when transplanted into immunodeficient recipients, supporting a two-pathway model for B lymphopoiesis, fetal “B-1” and adult “B-2”. Recently Lin28b was shown to be important for the switch between fetal and adult pathways; however, neither the mechanism of Lin28b action nor the importance of BCR signaling in this process was addressed. Here we report important advances in our understanding of the regulation of B 1/B-2 development. First, modulation of Let-7 in fetal Pro-B cells is sufficient to alter fetal B-1 development to produce B cells resembling the progeny of adult B-2 development. Second, intact BCR signaling is required for generation of B1a B cells from Lin28b-transduced bone marrow progenitors, supporting a requirement for ligand-dependent selection, as is the case for normal B1a B cells. Third, the VH repertore of Lin28b-induced bone marrow B1a B cells differs from that of normal B1a. Finally we identify the Arid3a transcription factor as a key target of Let-7, whose ectopic expression is sufficient to induce B-1 development in adult Pro-B cells and whose knockdown blocks B-1 development in fetal Pro-B cells. 2 individual sorts of bone marrow Pro-B cells 4 days after Lin28b retroviral transduction (and 2 sorts of empty vector control) and 2 individual sorts of fetal liver Pro-B cells 4 days after Let-7b retroviral transduction (and 2 sorts of empty vector controls).

2015-03-01 | E-GEOD-65534 | biostudies-arrayexpress

The OTUD6B-LIN28B-MYC axis determines cell cycle progression in multiple myeloma

Project description:Deubiquitylases (DUBs) remove ubiquitin from proteins. In the context of cancer, their inhibition can induce the degradation of oncoproteins, that may otherwise be “undruggable”. Multiple myeloma (MM) is the second most common hematological malignancy with poor outcome and high sensitivity towards ubiquitin-proteasome-system (UPS) inhibitory therapies. However, the role of DUBs in MM pathophysiology and therapy has remained elusive. Starting from genetic screening for DUB dependencies in MM, we here identify OTUD6B as a central vulnerability in MM that drives the G1/S cell cycle transition by means of deubiquitylating and stabilizing LIN28B subsequent to LIN28B phosphorylation. LIN28B regulates miRNA biogenesis and exerts high expression in embryonic stem cells that becomes re-established in certain tumors, including MM. Binding of LIN28B at G1/S activates OTUD6B, which otherwise remains in a catalytically inactive state. As a consequence, stabilized LIN28B drives MYC expression via inhibition of let7 microRNAs, which in turn allows for a rapid transition of MM cells from G1 to S phase. Analyses of primary MM patient samples reveal a positive correlation of OTUDB6B expression with poor outcome, high MYC expression and MYC target gene induction, suggesting that high MYC levels in MM result from an activation of the OTUD6B-LIN28B nexus. Together, we here specify phosphorylation and cell cycle-dependent substrate binding as a means by which OTUD6B becomes activated to drive the G1/S transition via the LIN28B-MYC axis and nominate OTUD6B and LIN28B as actionable vulnerabilities in MM.

2022-10-12 | PXD027480 | Pride

Gene expression profiling in LoVo-P compared with LoVo-C cells

Project description:The differential expression of mRNA in LoVo-P cells compared with LoVo-C cells was successfully detected using the Arraystar Human LncRNA/mRNAArray V4.0, that used for the global profiling of 20730 human mRNA and 40173 long non-coding RNA (LncRNA) transcripts.

2017-09-20 | GSE103989 | GEO

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