Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

PARVA promotes invasion through inducing phosphorylation of ILK signaling in lung cancer

ABSTRACT: Alpha-parvin (PARVA) is known to involve in the linkage of integrins, regulation of actin cytoskeleton dynamics, and cell survival. However, the role of PARVA in cancer progress is still unclear. Here, we identify PARVA as a potential oncogene from a lung cancer invasion cell line model by expression microarrays. Overexpression of PARVA enhances cell invasion, colony formation ability, and endothelial cell tube formation but knockdown of PARVA inhibits invasion and tube formation in vitro. PARVA also promotes tumorigenicity, angiogenesis, metastasis and mortality by in vivo tumorigenesis and metastasis mouse models. To explore the underlying mechanism, the PARVA-regulated signaling pathways were analyzed in PARVA-overexpressing cells compare with mock controls by expression microarrays. We used microarrays to profile the global gene expression of PARVA-overexpressing cells compared with mock control cells and identified the pathways involved in PARVA-induced biofunctional alterations.

ORGANISM(S): Homo sapiens

PROVIDER: GSE50657 | GEO | 2016/08/25

SECONDARY ACCESSION(S): PRJNA218205

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Similar Datasets

HOXA5 inhibits metastasis and associates with prolonged survival in lung cancer

Project description:Homeobox genes comprise a family of regulatory genes that contain a common homeobox domain and act as transcription factors. Changes in the expression of homeobox genes are observed in many cancers, including leukaemia, colon, skin, prostate, breast, and ovarian cancers. Recent studies indicate that homeobox A5 (HOXA5) may serve as a tumour suppressor gene in breast cells. However, the precise role of HOXA5 in lung cancer remains unclear. Using microarrays and an invasion/metastasis lung adenocarcinoma cell line model, we showed that the expression of HOXA5 is negatively correlated with cancer cell invasion ability. The ectopic expression of HOXA5 in highly invasive cancer cells suppressed cell migration, invasion, and filopodia formation in vitro and inhibited metastatic potential in vivo. The knockdown of HOXA5 expression via a HOXA5-specific siRNA was able to promote the invasiveness of lung cancer cells. Furthermore, HOXA5 expression was associated with improved overall survival and disease-free survival in non-small cell lung cancer patients with wild-type EGFR (P = 0.0199 and 0.0345, respectively). Genome-wide transcriptome and pathway analyses indicated that these effects of HOXA5 may be associated with the regulation of cytoskeletal remodelling. In summary, our studies provide new insights into how HOXA5 may contribute to the suppression of metastasis in lung cancer. We used microarrays to profile the global gene expression of HOXA5-overexpressing cells compared with mock control cells and identified the pathways involved in HOXA5-induced biofunctional alterations.

2016-08-25 | GSE50659 | GEO

WTAP-induced change in gene expresssion in cholangiocarcinoma cells

Project description:Knock-down or overexpression of WTAP regulated migration and invasion of cholangiocarcinoma cells in vivo and vitro studies. To investigate the underlying mechanism for WTAP-regulated migration and invasion, the gene expression between the mock cells and the stable cells was compared Total RNA was purified from the mock cells and the stable cells overexpressing WTAP

2015-04-06 | E-GEOD-32134 | biostudies-arrayexpress

LAP2beta-induced change in gene expression in gastric cancer cells

Project description:Knock-down or overexpression of LAP2beta regulated migration and invasion of gastric cancer cells in vivo and in vitro studies. To investigate the underlying mechanism for LAP2beta-regulated migration and invasion, we compared the gene expression changes between the mock cells and the stable cells. Total RNA was purified from the mock cells and the stable cells overexpressing LAP2beta

2012-07-31 | E-GEOD-31450 | biostudies-arrayexpress

CHD5 inhibits metastasis of neuroblastoma

Project description:CHD5, a tumor suppressor at 1p36, is frequently lost or silenced in poor prognosis neuroblastoma (NB) and many adult cancers. The role of CHD5 in metastasis is unknown. We confirm that low expression of CHD5 is associated with stage 4 NB. Forced expression of CHD5 in NB cell lines with 1p loss inhibited key aspects of the metastatic cascade in vitro: anchorage-independent growth, migration and invasion. In vivo, formation of bone marrow and liver metastases developing from intravenously injected NB cells was delayed and decreased by forced CHD5 expression. Genome-wide mRNA sequencing revealed reduction of genes and gene sets associated with metastasis when CHD5 was overexpressed. Known metastasis-suppressing genes preferentially up-regulated in CHD5-overexpressing NB cells included PLCL1. In patient NB, low expression of PLCL1 was associated with metastatic disease and poor survival. Knock-down of PLCL1 and of p53 in IMR5 NB cells overexpressing CHD5 reversed CHD5-induced inhibition of invasion and migration in vitro. In summary, CHD5 is a metastasis suppressor in NB.

2021-09-11 | GSE183824 | GEO

Expression data from RECK-overexpressing HT1080 fibrosarcoma cells

Project description:RECK, a glycosylphosphatidylinositol-anchored glycoprotein, inhibits the enzymatic activities of some matrix metalloproteinases (MMP), thereby suppressing tumor cell metastasis; however, the detailed mechanism is still obscure. In this study, we compared the gene expression profiles between mock- and RECK-transfected HT1080 cells. Three established cell lines were selected for RNA extraction and hybridization on Affymetrix microarrays: (1) mock-transfected HT1080 cells, designated as HT1080-Zeo, (2) RECK-overexpressing HT1080 cells, designated as HT1080-RECK, and (3) RECK/4NQ-overexpressing HT1080 cells (in which four N-glycosylation asparagine residues of RECK (Asn86, Asn200, Asn297, and Asn352) were replaced with glutamine residues), designated as HT1080-RECK/4NQ.

2010-04-14 | E-GEOD-21306 | biostudies-arrayexpress

miRNA Expression data from WASF3 overexpressing stable T47D cells and control cells

Project description:We recently showed that inactivation of the WASF3/WAVE3 gene in breast cancer cells results in loss of cell motility and invasion in vitro and metastasis in vivo. To obtain a better understanding of molecular mechanisms of action of WASF3, we have established the stable WASF3 overexpressing T47D cells using lentiviral infect system. We used miRNA microarrays to detail the global programme of miRNA expression after overexpression of WASF3 and identified distinct classes of up or down-regulated metastmir associated with breast cancer cell migration and motility invasion

2014-08-19 | GSE31367 | GEO

Transcriptome profiling of renal glomeruli from Parva-fl/fl*hNPHS2Cre and WT mice

Project description:Podocyte specific knockout mice for Parva (Parva-fl/fl*hNPHS2Cre) were generated. Transcriptome profiling (RNA-Seq) and differential gene expression analysis of isolated renal glomeruli from KO and WT mice was performed. Parva KO mice showed transcriptional changes associated with podocyte and glomerular disease.

2022-01-20 | GSE181690 | GEO

Expression data from G9a overexpression and knockdown lung cancer cell lines

Project description:G9a is the major mammalian H3-K9 methyltransferase that targets euchromatic regionsand is essential for murine embryogenesis . We demonstrate that G9a is endowed with methyltransferase activity to concomitantly repress the downstream effector Ep-CAM, thereby promoting the invasion step of the invasion-metastasis cascade. We used microarrays to detail the G9a regulated gene expression underlying invasion-metastasis cascade and identified distinct classes of up-regulated genes during this process.

2011-12-31 | GSE22810 | GEO

Expression data from G9a overexpression and knockdown lung cancer cell lines

2011-12-31 | E-GEOD-22810 | biostudies-arrayexpress

EphA6 promotes angiogenesis and prostate cancer metastasis and is associated with human prostate cancer progression

Project description:Purpose: Metastasis remains the primary cause of prostate cancer (CaP) related death. Here, we investigate the molecular, pathologic, and clinical outcome associations of EphA6 expression and its role in CaP progression and metastasis.Experimental Design: The gene expression profiling of Eph receptors (Ephs) and their ephrin ligands was performed in CaP cell lines by real-time RT-PCR. Metastatic potential of EphA6 gene was analyzed by RNAi approaches in a spontaneous CaP mouse model. The mRNA expression of EphA6 was measured in 58 benign prostate hyperplasia (BPH) and 112 CaP samples. Results: Among the tested Ephs and ligands, EphA6 is the only consistently overexpressed member in CaP lymph node metastatic cells. EphA6 knock-down (KD) in human PC-3M cells causes decreased invasion in vitro and reduced lung and lymph node metastasis in vivo. In addition, KD of EphA6 decreases tube formation in vitro and angiogenesis in vivo. Studies on the clinical samples demonstrate that EphA6 is overexpressed in the CaP tumor tissues compared with those from BPH patients. The correlation was identified between EphA6 expression and vascular invasion (P=0.004), neural invasion (P=0.002), PSA level (P=0.013), and TNM staging (P=0.021) in 112 CaP cases.Further, genome-wide gene expression analysis in KD of EphA6 cells identified a panel of genes, such as PIK3IPA, AKT1, and EIF5A2, which could be associated with EphA6-regulated cancer progression. Conclusions: These findings identify EphA6 as a potentially novel metastasis gene, and increased EphA6 mRNA expression positively correlates with CaP progression. The mechanisms to inhibit EphA6 expression might suppress CaP metastatic aggressiveness. Knock-down of EphA6 induced gene expression in human prostate cell:PC-3M/shEphA6-1, PC3M/shControl, CWR22rv1/shEphA6-1, and CWR22rv1/shControl cell line.

2015-02-27 | E-GEOD-66335 | biostudies-arrayexpress

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

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