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Expression data from Snail over-expressing non-small cell lung cancer cell lines

ABSTRACT: Snail is a zinc-finger transcription factor best known for its ability to down-regulate E-cadherin. Its established significance in embryology and organogenesis has been expanded to include a role in the tumor progression of a number of human cancers. In addition to E-cadherin, it has more recently been associated with the down-regulation and up-regulation of a number of other genes that affect important malignant phenotypes. After establishing the presence of up-regulated Snail in human non-small cell lung cancer specimens, we used microarrays to detail the global programme of gene expression in non-small cell lung cancer cell lines stably transduced to over-express Snail as compared to vector control cell lines.

ORGANISM(S): Homo sapiens

PROVIDER: GSE16194 | GEO | 2010/05/21

SECONDARY ACCESSION(S): PRJNA117205

REPOSITORIES: GEO

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Expression data from Snail over-expressing non-small cell lung cancer cell lines

Project description:Snail is a zinc-finger transcription factor best known for its ability to down-regulate E-cadherin. Its established significance in embryology and organogenesis has been expanded to include a role in the tumor progression of a number of human cancers. In addition to E-cadherin, it has more recently been associated with the down-regulation and up-regulation of a number of other genes that affect important malignant phenotypes. After establishing the presence of up-regulated Snail in human non-small cell lung cancer specimens, we used microarrays to detail the global programme of gene expression in non-small cell lung cancer cell lines stably transduced to over-express Snail as compared to vector control cell lines. Non-small cell lung cancer cell lines (H441, H292, H1437) were stably transduced with a retroviral vector to over-express Snail. Elevated Snail and a corresponding down-regulation of E-cadherin was verified in the Snail over-expressing cell lines as compared to vector control cell lines by Western analysis. RNA extraction was performed and samples submitted to the UCLA Clinical Microarray Core for hybridization to Affymetrix arrays.

2010-06-08 | E-GEOD-16194 | biostudies-arrayexpress

Title: Non-canonical functions of SNAIL drive context-specific progression

Project description:SNAIL is a key transcriptional regulator in embryonic development and cancer. Its effects in physiology and disease are believed to be linked to its role as a master regulator of epithelial-to-mesenchymal transition (EMT). Here, we report EMT-independent oncogenic SNAIL functions in cancer. Using genetic models, we systematically interrogated SNAIL effects in various oncogenic backgrounds and tissue types. SNAIL related phenotypes displayed remarkable tissue- and genetic context-dependencies, ranging from protective effects as observed in KRAS- or WNT-driven intestinal cancers, to dramatic acceleration of tumorigenesis, as shown in KRAS-induced pancreatic cancer. Unexpectedly, SNAIL-driven oncogenesis was not associated with E-cadherin downregulation or induction of an overt EMT program. Instead, we show that SNAIL induces bypass of senescence and cell cycle progression through p16INK4A-independent inactivation of the Retinoblastoma (RB)-restriction checkpoint. Collectively, our work identifies novel non-canonical EMT-independent functions of SNAIL and unravel its complex context-dependent role in cancer.

2022-12-13 | PXD038726 | Pride

MicroRNA response to Snail overexpression in lung cancer cell lines

Project description:Analysis of four lung cancer cell lines transfected with a vector expressing the transcriptional repressor Snail versus a vector control. Aberrant Snail expression is known to induce an EMT program in lung cancers.

2013-07-17 | GSE48922 | GEO

The influence of Snail expression on mRNA transcription levels in II-18 cells

2010-05-03 | GSE19679 | GEO

Snail-dependent epithelial splicing regulatory protein 1 (ESRP1) silencing drives malignant transformation of human pulmonary epithelial cells [miRNA]

Project description:The significance of epithelial-to-mesenchymal transition (EMT)-inducing transcription factors in the onset of non-small cell lung cancer has not been resolved. Here, we report increased Snail expression in pulmonary premalignant lesions relative to histologically normal-appearing pulmonary epithelium. Utilizing immortalized human pulmonary epithelial cells and isogenic derivatives, we document Snail-dependent anchorage-independent growth of the epithelial cells in vitro, as well as transformation, primary tumor growth, and metastatic behavior in vivo. Epithelial splicing regulatory protein 1 (ESRP1) tumor suppressor silencing was a requirement for Snail-driven transformation in vivo, and we identified ESRP1 loss in Snail-expressing pulmonary premalignant lesions in situ. Snail drives these and other carcinogenic signaling programs in an ALDH+CD44+CD24- pulmonary stem cell subset in which ESRP1 and stemness-repressing micro-RNAs are inhibited.

2017-12-16 | GSE108136 | GEO

Snail-dependent epithelial splicing regulatory protein 1 (ESRP1) silencing drives malignant transformation of human pulmonary epithelial cells [mRNA]

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The mRNA expression of FaDu-Ctrl, FaDu-Snail, FaDu-Snail2R cells

Project description:To screen the genes regulated by wt-Snail and non-acetylated Snail The successful development of cancer metastasis requires two major events: the reprogramming of cancer cells to increase their migration and tumor-initiation capabilities; and the remodeling of the tumor microenvironment to facilitate invasion and colonization of cancer cells. Epithelial-mesenchymal transition (EMT) is a crucial mechanism for reprogramming cancer cells to possess tumor initiation and migration capabilities1,2. However, the role of EMT in the interplay between tumor and host cells is largely unknown. The EMT regulator Snail is mainly known as a transcriptional repressor of the adhesion protein E-cadherin, whose repression is considered to be a key step in initiating metastasis3,4. We previously found that Snail can also act as an activator that induces the transcription of ERCC15 and IL86. Here we show that Snail is acetylated by CREB-binding protein (CBP) and that Snail and CBP co-occupy the promoters of target genes to activate transcription of the target genes. Furthermore, Snail activates the expression of a panel of cytokine genes, including TNFa (which forms a positive feedback loop with Snail to amplify the signal) and CCL2 and CCL5 (which facilitate the recruitment of macrophages by cancer cells). Our results demonstrate a novel function for Snail, providing new understanding of the recruitment of host cells to tumor sites during metastatic evolution.

2014-08-16 | GSE58592 | GEO

The influence of Snail expression on mRNA transcription levels in II-18 cells

Project description:Snail is a transcriptional repressor, which induces epithelial-mesenchymal transition. However, overall functions of Snail remain to be elucidated. This microarray was performed to investigate the influence of Snail expression on mRNA transcription levels in a lung adenocarcinoma cell line, II-18. II-18 cells were infected by retrovirus vectors expressing Snail or control vectors at a multiplicity of infection of 50-100. After 5 days postinfection, total RNA was obtained from II-18 cells expressing Snail (3 samples) or control II-18 cells (3 samples).

2010-05-27 | E-GEOD-19679 | biostudies-arrayexpress

4T1 cells with Control vs SNAIL vs SNAIL/FBXO11

Project description:Transcriptional profiling of mouse 4T1 breast cancer cells stably tranduced with pLEX-MCS based lentivirus. Three groups were compared, Vector cells, SNAIL expressing cells; and SNAIL+FBXO11 expressing cells. SNAIL expression induced strong EMT phenotype while SNAIL/FBXO11 reversed cells back to epithelial cells.

2014-12-01 | GSE50887 | GEO

Expression data from gastric cancer cell line HGC27 after knockdown of SNAIL

Project description:SNAIL, which is a key factor in EMT, has high expression levels in the gastric spheres. To investigate SNAIL-regulated genes, we knocked down this gene in the gastric cancer cell line HGC-27 and compared the gene expression of these cells with those of the parental cells by microarray.

2020-02-25 | GSE145867 | GEO

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