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TRPM7 maintains progenitor-like features of neuroblastoma cells

ABSTRACT: Analysis of the effect of shRNA-mediated knockdown of TRPM7 on gene expression levels in SH-SY5Y and SH-EP2 human neuroblastoma cells. Results were used for the identification of neural-crest-associated transcription factors that were affected by TRPM7 knockdown.

ORGANISM(S): Homo sapiens

PROVIDER: GSE64000 | GEO | 2014/12/10

SECONDARY ACCESSION(S): PRJNA269742

REPOSITORIES: GEO

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TRPM7 maintains progenitor-like features of neuroblastoma cells

Project description:Analysis of the effect of shRNA-mediated knockdown of TRPM7 on gene expression levels in SH-SY5Y and SH-EP2 human neuroblastoma cells. Results were used for the identification of neural-crest-associated transcription factors that were affected by TRPM7 knockdown. Total RNA isolated from SH-EP2 and SH-SY5Y human neuroblastoma cells transduced with a scrambled shRNA (control) or TRPM7 shRNA, experiment performed in duplicate.

2014-12-10 | E-GEOD-64000 | biostudies-arrayexpress

TRPM7 maintains mesenchymal phenotype of breast cancer cells by tensional regulation of SOX4 (TRPM7 shRNA)

Project description:Analysis of the effect of shRNA-mediated knockdown of TRPM7 on gene expression levels in MDA-MB-231 human breast cancer cells. Results were used for the identification of so-called epithelial-mesenchymal transcription factors that were affected by TRPM7 knockdown and for the analysis of overlapping up- and downregulated genes in shT7#1 + shSOX4#1 MDA-MB-231 cells

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TRPM7 maintains mesenchymal phenotype of breast cancer cells by tensional regulation of SOX4 (SOX4 shRNA)

Project description:Analysis of the effect of shRNA-mediated knockdown of SOX4 on global gene expression levels in MDA-MB-231 human breast cancer cells. Results were used for the identification of overlapping up- and downregulated genes in TRPM7 + SOX4 shRNA MDA-MB-231 cells

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TRPM7 maintains progenitor-like features of neuroblastoma cells: implications for metastasis formation.

Project description:Neuroblastoma is an embryonal tumor derived from poorly differentiated neural crest cells. Current research is aimed at identifying the molecular mechanisms that maintain the progenitor state of neuroblastoma cells and to develop novel therapeutic strategies that induce neuroblastoma cell differentiation. Mechanisms controlling neural crest development are typically dysregulated during neuroblastoma progression, and provide an appealing starting point for drug target discovery. Transcriptional programs involved in neural crest development act as a context dependent gene regulatory network. In addition to BMP, Wnt and Notch signaling, activation of developmental gene expression programs depends on the physical characteristics of the tissue microenvironment. TRPM7, a mechanically regulated TRP channel with kinase activity, was previously found essential for embryogenesis and the maintenance of undifferentiated neural crest progenitors. Hence, we hypothesized that TRPM7 may preserve progenitor-like, metastatic features of neuroblastoma cells. Using multiple neuroblastoma cell models, we demonstrate that TRPM7 expression closely associates with the migratory and metastatic properties of neuroblastoma cells in vitro and in vivo. Moreover, microarray-based expression profiling on control and TRPM7 shRNA transduced neuroblastoma cells indicates that TRPM7 controls a developmental transcriptional program involving the transcription factor SNAI2. Overall, our data indicate that TRPM7 contributes to neuroblastoma progression by maintaining progenitor-like features.

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