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Roles of Snail-regulated miRNAs in colon cancer progression

ABSTRACT: The transcription factor Snail is known as an EMT regulator to promote cancer metastasis. Identification Snail-regulated miRNAs helps to uncover mechanisms governing CRC metastasis

ORGANISM(S): Homo sapiens Primates

PROVIDER: GSE39286 | GEO | 2013/11/20

SECONDARY ACCESSION(S): PRJNA170855

REPOSITORIES: GEO

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Roles of Snail-regulated miRNAs in colon cancer progression

Project description:The transcription factor Snail is known as an EMT regulator to promote cancer metastasis. Identification Snail-regulated miRNAs helps to uncover mechanisms governing CRC metastasis The stable SW480-vector and Snail-expressing cells were established for miRNA microarray analysis.

2013-11-20 | E-GEOD-39286 | 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

Ovarian cancer cell line response to Snail depletion

Project description:Analysis of mouse ovarian cancer cell line HM-1 transfected with shRNA targeting Snail, an EMT inducer. Anti-tumor immuty in state of EMT remains unclear. We focused on Snail, a major EMT inducer, and explored the influence of Snail on immune ivasion into ovarian tumors by generating Snail knockdown cell line. Elucidating the mechanisms of Snail-induced immune evasion will lead to the development of novel treatment strategies for tumor undergoing EMT.

2018-01-27 | GSE109688 | GEO

HMLEN cells with Vector Control vs SNAIL vs SNAIL/FBXO11

Project description:Transcriptional profiling of mouse HMLEN breast cancer cells (HMLE cells transformed with -Neu oncogene) 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 | GSE50888 | GEO

Transcriptome of EMT induced MCF10A cells by TGFb treatment or SNAIL S6A expression.

Project description:EMT, Epithelial to mesenchymal transition is a developmental biology process associated with migration, known to be involved in cancer metastasis. To study this process, we used the breast epithelial cell line MCF10A that enter in EMT after treatment with the cytokine TGFB or by expression of EMT transcriptor factor SNAIL.

2017-01-30 | GSE89152 | GEO

Dynamic Chromatin Modification Sustains Epithelial-Mesenchymal Transition following Inducible Expression of Snail-1 (gene expression)

Project description:Epithelial-Mesenchymal Transition (EMT) is thought to contribute to cancer metastasis, but its underlying mechanisms are not well understood. To define early steps in this cellular transformation, we analyzed human mammary epithelial cells with tightly regulated expression of Snail-1, a master regulator of EMT. Following Snail-1 induction, epithelial markers were repressed within 6 hours and mesenchymal genes induced at 24 hours. Snail-1 binding to its target promoters was transient (6-48 hours) despite continued protein expression and it was followed by both transient and long-lasting chromatin changes.

2013-12-18 | GSE52592 | GEO

Dynamic Chromatin Modification Sustains Epithelial-Mesenchymal Transition following Inducible Expression of Snail-1 (ChIP-chip)

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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. Establish stable transfectants of pCDH-Snail and pCDH-Snail2R in FaDu cells and analyze the mRNA expression level of by cDNA microarray. FaDu transfected with pCDH vector was used as a control experiment.

2014-08-16 | E-GEOD-58592 | biostudies-arrayexpress

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

2014-08-16 | GSE58592 | GEO

Snail and Twist expression in HMLE and MCF10A cells

Project description:Snail and Twist are two EMT inducer, expression of Snail or Twist will induce EMT in HMLE and MCF10A cells. By introducing Snail or Twist in HMLE and MCF10A cells, which lack the expression of these two proteins, will identify the genes are induced during EMT. We used microarray analysis to compare the gene expression profiles between the mammamry epithleial cells and the cells undergone EMT.

2020-01-10 | GSE143349 | GEO

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