E-GEOD-20318
Ontology highlight
ABSTRACT:
OTHER RELATED OMICS DATASETS IN: PRJNA125375
PROVIDER: E-GEOD-20318 | ExpressionAtlas | 2015-08-07
REPOSITORIES: ExpressionAtlas
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| E-GEOD-20318-analysis-methods.tsv | Tabular | |||
| E-GEOD-20318-atlasExperimentSummary.Rdata | Rdata | |||
| E-GEOD-20318-configuration.xml | Xml | |||
| E-GEOD-20318-percentile-ranks.tsv | Tabular | |||
| E-GEOD-20318.condensed-sdrf.tsv | Tabular |
Items per page: 5 1 - 5 of 53 |
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Project description:Metastasis is a major cause leading to mortality for lung cancer patients. We identified YWHAZ as a potential metastasis-promoting candidate and found that overexpression of YWHAZ promotes lung cancer cell proliferation, anchorage-independent growth, migration, and invasion in vitro, as well as tumorigenesis and metastasis in vivo. It not only increases cell protrusions and branchings but also induces epithelial-mesenchymal transition. Most importantly, YWHAZ protein could prevent £]-catenin from ubiquitination via its association with £]-catenin and enhance slug transcriptional activity which is regulated by £]-catenin/TCF signaling pathway. Moreover, YWHAZ expression was higher in tumors than in adjacent normal tissues in 63 Non-small-cell lung cancer (NSCLC) patients. NSCLC patients with high YWHAZ expressing tumors had shorter overall survival than those with low-expressing tumors. We conclude that YWHAZ play a critical role in promoting NSCLC metastasis. In this investigation, we used a lung cancer invasion cell model to identify the genes involved in cancer progression. YWHAZ is a potential oncogene whose expression is correlated to the survival of patients with breast, prostate and liver cancers. However, the role of YWHAZ in lung caner progression has not been reported, particularly in metastasis. Here, YWHAZ was ectopically expressed in lower invasive lung cancer cell line its impact on colonogenesis, migration and invasiveness was assessed. The underlying mechanism was explored by YWHAZ-expressed transfectants and microarrays and the clinical relevance was evaluated by quantitative RT-PCR.
2012-11-07 | E-GEOD-20318 | biostudies-arrayexpress
Project description:Identifying patients at risk for metastatic relapse is a critical need in oncology. We identified a common missense germline variant in PCSK9 (rs562556) that associates with reduced breast cancer survival outcomes in multiple cohorts. Genetic modeling of this gain-of-function single nucleotide variant in mice revealed that it causally promoted breast cancer metastasis. Conversely, host PCSK9 deletion reduced metastatic colonization in multiple breast cancer models. Host PCSK9 promoted metastatic initiation events in lung and increased proliferative competence by targeting tumoral LRP1 receptors which repress metastasis-promoting genes. Antibody-mediated therapeutic inhibition of PCSK9 suppressed breast cancer metastasis in multiple models. rs562556 stratified women in a large Swedish early-stage breast cancer cohort into those with 98% versus 78% distant-metastasis-free interval at 15 years after diagnosis. Our findings reveal that a commonly inherited genetic alteration predicts breast cancer survival and governs breast cancer metastasis—uncovering a hereditary basis underlying a prevalent cause of mortality.
2024-12-05 | PXD049279 | Pride
Project description:Background: α-catulin may functions as an oncoprotein, sustaining proliferation by preventing cellular senescence and promoting cancer cell migration. In this study, we investigated the mechanism of α-catulin in cancer cell migration and metastasis in lung cancer. Method: α-catulin mRNA expression was isolated from A549/AS2neo (control) and A549/AS2neo-α-catulin stable cells. The Phalanx Human OneArray microarray analysis was performed to identify α-catulin downstream genes. Results: Overexpression of α-catulin increased cancer cell migration and metastasis. By using Phalanx Human OneArray microarray we have identified panel of genes altered by α-catulin overexpression, consisting of CDC42, intergrins and genes related to cytoskeleton remodeling. Conclusion: α-catulin is an oncoprotein and promotes lung cancer cell migration and metastasis. Two-condition experiment, Vector vs. alpha-catulin overexpression cells.The cDNAs encoding full-length human alpha-catulin were amplified and subcloned into lentiviral pLKO_AS2.neo which generated full-length alpha-catulin. Vector control or alpha-catulin lentivirus were transduced into A549 cells and G418 was used to select stable cells.
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Project description:Background: α-catulin may functions as an oncoprotein, sustaining proliferation by preventing cellular senescence and promoting cancer cell migration. In this study, we investigated the mechanism of α-catulin in cancer cell migration and metastasis in lung cancer. Method: α-catulin mRNA expression was isolated from A549/AS2neo (control) and A549/AS2neo-α-catulin stable cells. The Phalanx Human OneArray microarray analysis was performed to identify α-catulin downstream genes. Results: Overexpression of α-catulin increased cancer cell migration and metastasis. By using Phalanx Human OneArray microarray we have identified panel of genes altered by α-catulin overexpression, consisting of CDC42, intergrins and genes related to cytoskeleton remodeling. Conclusion: α-catulin is an oncoprotein and promotes lung cancer cell migration and metastasis.
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Project description:Background: JAG-1 is a ligand of Notch signaling and can regulate cell differentiation and proliferation in cancers. Recent studies indicated that JAG1 is a gene associated with cancer progression. Therefore, we investigated the role of JAG1 in lung cancer progression. Methods: The expression of JAG1 was manipulated by overexpression or RNA silencing in several human lung cell lines. The effect of JAG1 on tumorigenesis and invasion was assessed by the cell anchorage-independent growth, cell proliferation, cell migration and invasion assays in vitro as well as metastasis in vivo. The potential downstream genes of JAG1 were identified by oligonucleotide microarrays and quantitative reverse transcription¡Vpolymerase chain reaction (RT-PCR). We further measured JAG1 expression in lung cancer specimens by RT-PCR. Correlation between JAG1 expression and overall survival of lung cancer patients was determined by using the log-rank test and multivariable Cox proportional hazards regression analysis. All statistical tests were two-sided. Results: JAG1 enhanced anchorage-independent growth, cell migration, invasion in the lower invasive cells, CL1-0. JAG1 also increased the capability of migration and invasion in the other two lung cancer cell lines (A549 and NCI-H226). The silencing of JAG1 inhibited migration and invasion activities of the higher invasive cells, CL1-5, by siRNA technology. The invasion-promoting activity of JAG1 was also demonstrated in vivo by using a mouse metastasis model. By microarray analysis, we found that the expression of heat shock 70kDa protein 2 (HSPA2) was activated by JAG1 overexpression and eliminated by JAG1 silencing. Moreover, lung cancer patients with high JAG1 expressing tumors had shorter overall survival than those with low-expressing tumors. Conclusion: JAG1 might be an oncogene which promotes colonogenesis and metastasis, and high JAG1 expression is associated with shorten survival in lung cancer. In this investigation, we used a lung cancer invasion cell model to identify the genes involved in cancer progression. JAG1 is a potential oncogene whose expression is correlated to the survival of patients with breast, prostate and liver cancers. However, the role of JAG1 in lung caner progression has not been reported, particularly in metastasis. Here, JAG1 was ectopically expressed in lower invasive lung cancer cell line its impact on colonogenesis, migration and invasiveness was assessed. The underlying mechanism was explored by JAG1-expressed transfectants and microarrays and the clinical relevance was evaluated by quantitative RT-PCR.
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