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Genome-wide maps of SNAI2 binding in undifferentiated and differentiated keratinocytes

ABSTRACT: We report the ChIP-Seq results of SNAI2 in several different conditions which include: SNAI2 binding in both control and SNAI2 knockdown cells to demonstrate specificity of the binding. SNAI2 ChIP-Seq was also performed in SNAI2 or control LACZ overexpressing cells cultured in growth medium as well as LACZ or SNAI2 overexpressing cells in differentiation medium.

ORGANISM(S): Homo sapiens

PROVIDER: GSE55421 | GEO | 2014/10/15

SECONDARY ACCESSION(S): PRJNA239547

REPOSITORIES: GEO

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Genome-wide maps of SNAI2 binding in undifferentiated and differentiated keratinocytes

Project description:We report the ChIP-Seq results of SNAI2 in several different conditions which include: SNAI2 binding in both control and SNAI2 knockdown cells to demonstrate specificity of the binding. SNAI2 ChIP-Seq was also performed in SNAI2 or control LACZ overexpressing cells cultured in growth medium as well as LACZ or SNAI2 overexpressing cells in differentiation medium. Examination of SNAI2 binding sites across the genome using the 6 different conditions

2014-10-15 | E-GEOD-55421 | biostudies-arrayexpress

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Gene expression data on human keratinocytes with knockdown or overexpression of SNAI2

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Project description:This experiment shows differential expression of genes in the luminal, basal and stromal subpopulations from SNAI2+/+ and SNAI2 LacZ/LacZ mammary epithelial cells.

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Project description:Investigation of the transcriptional profile of SNAI2-overexpressing HaCaT cells.

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PARP1-SNAI2 Transcription Axis Drives Resistance to PARP Inhibitor, Talazoparib

Project description:The synthetic lethal association between BRCA deficiency and poly (ADP-ribose) polymerase (PARP) inhibition supports PARP inhibitor (PARPi) clinical efficacy in BRCA-mutated tumors. PARPis also demonstrate activity in non-BRCA mutated tumors presumably through induction of PARP1-DNA trapping. Despite pronounced clinical response, therapeutic resistance to PARPis inevitably develops. An abundance of knowledge has been built around resistance mechanisms in BRCA-mutated tumors, however, parallel understanding in non-BRCA mutated settings remains insufficient. In this study, we find a strong correlation between the epithelial-mesenchymal transition (EMT) signature and resistance to a clinical PARPi, Talazoparib, in non-BRCA mutated tumor cells. Genetic profiling demonstrates that SNAI2, a master EMT transcription factor, is transcriptionally induced by Talazoparib treatment or PARP1 depletion and this induction is partially responsible for the emerging resistance. Mechanistically, we find that the PARP1 protein directly binds to SNAI2 gene promoter and suppresses its transcription. Talazoparib treatment or PARP1 depletion lifts PARP1-mediated suppression and increases chromatin accessibility around SNAI2 promoters, thus driving SNAI2 transcription and drug resistance. We also find that depletion of the chromatin remodeler CHD1L suppresses SNAI2 expression and reverts acquired resistance to Talazoparib. The PARP1/CHD1L/SNAI2 transcription axis might be therapeutically targeted to re-sensitize Talazoparib in non-BRCA mutated tumors.

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Project description:The prognosis of pancreatic cancer is still poor due to resistance to conventional therapies, and cancer stem cells (CSCs) targeted therapy is expected to be a promising therapy. Although epithelial mesenchymal transition-inducing transcription factors (EMT-TF) are known to impart the CSCs properties to some of solid tumors, it has not been clearly reported in pancreatic cancer yet. Zinc finger protein SNAI2, a member of the Snail superfamily of EMT-TF, is frequently overexpressed in pancreatic cancer cells and the poor prognosis has been reported in cases with high SNAI2 expression. we found the suppression of SNAI2 expression using RNA interference decreased the tumorigenicity in vitro (sphere formation assay) as well as in vivo (xenograft assay) in the pancreatic cancer cell line KLM1. Furthermore, microarray analysis suggests that the mechanism is mediated by insulin-like growth factor binding protein 2 (IGFBP2). These results indicate that SNAI2 may be a critical factor for the CSCs properties and indispensable for the homeostasis of pancreatic CSCs.

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