Roles of Snail-regulated miRNAs in colon cancer progression
Ontology highlight
ABSTRACT:
ORGANISM(S): Primates Homo sapiens
PROVIDER: GSE39286 | GEO | 2013/11/20
SECONDARY ACCESSION(S): PRJNA170855
REPOSITORIES: GEO
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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.
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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.
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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.
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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.
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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.
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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.
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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.
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