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Identification and validation of novel ERBB2 (HER2, NEU) targets including genes

ABSTRACT: V-erb-b2 erythroblastic leukemia viral oncogene homolog 2 (ERBB2; synonyms HER2, NEU) encodes a transmembrane glycoprotein with tyrosine kinase-specific activity that acts as a major switch in different signal-transduction processes. ERBB2 amplification and overexpression have been found in a number of human cancers, including breast, ovary and kidney carcinoma. Our aim was to detect ERBB2- regulated target genes that contribute to its tumorigenic effect on a genomewide scale. The differential gene expression profile of ERBB2- transfected and wild-type mouse fibroblasts was monitored employing DNA microarrays. Regulated expression of selected genes was verified by RT-PCR and validated by Western blot analysis. Genomewide gene expression profiling identified (i) known targets of ERBB2 signaling, (ii) genes implicated in tumorigenesis but so far not associated with ERBB2 signaling as well as (iii) genes not yet associated with oncogenic transformation, including novel genes without functional annotation. We also found that at least a fraction of coexpressed genes are closely linked on the genome. ERBB2 overexpression suppresses the transcription of antiangiogenic factors (e.g., Sparc, Timp3, Serpinf1) but induces expression of angiogenic factors (e.g., Klf5, Tnfaip2, Sema3c). Profiling of ERBB2-dependent gene regulation revealed a compendium of potential diagnostic markers and putative therapeutic targets. Identification of coexpressed genes that colocalize in the genome may indicate gene regulatory mechanisms that require further study to evaluate functional coregulation.

ORGANISM(S): Mus musculus

PROVIDER: GSE16445 | GEO | 2009/06/10

SECONDARY ACCESSION(S): PRJNA116349

REPOSITORIES: GEO

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Identification and validation of novel ERBB2 (HER2, NEU) targets including genes

Project description:V-erb-b2 erythroblastic leukemia viral oncogene homolog 2 (ERBB2; synonyms HER2, NEU) encodes a transmembrane glycoprotein with tyrosine kinase-specific activity that acts as a major switch in different signal-transduction processes. ERBB2 amplification and overexpression have been found in a number of human cancers, including breast, ovary and kidney carcinoma. Our aim was to detect ERBB2- regulated target genes that contribute to its tumorigenic effect on a genomewide scale. The differential gene expression profile of ERBB2- transfected and wild-type mouse fibroblasts was monitored employing DNA microarrays. Regulated expression of selected genes was verified by RT-PCR and validated by Western blot analysis. Genomewide gene expression profiling identified (i) known targets of ERBB2 signaling, (ii) genes implicated in tumorigenesis but so far not associated with ERBB2 signaling as well as (iii) genes not yet associated with oncogenic transformation, including novel genes without functional annotation. We also found that at least a fraction of coexpressed genes are closely linked on the genome. ERBB2 overexpression suppresses the transcription of antiangiogenic factors (e.g., Sparc, Timp3, Serpinf1) but induces expression of angiogenic factors (e.g., Klf5, Tnfaip2, Sema3c). Profiling of ERBB2-dependent gene regulation revealed a compendium of potential diagnostic markers and putative therapeutic targets. Identification of coexpressed genes that colocalize in the genome may indicate gene regulatory mechanisms that require further study to evaluate functional coregulation. Erbb2 transfected NIH3T3 cells versus un-transfected cells, 4 technical replicates including two colour swap experiments

2010-06-25 | E-GEOD-16445 | biostudies-arrayexpress

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Gene regulation in Erbb2 transfected NIH3T3 cells using tet-off system

2009-09-01 | E-GEOD-8373 | biostudies-arrayexpress

Genome-wide transcriptional profiling of Legionella Pneumophila-infected A549 cells transfected with siRNA against TNFAIP2

Project description:In this study we transfected A549 cells with siRNA against TNFAIP2, infected them with L. pneumophila and performed transcriptional profiling. We found enrichment of genes in pro-inflammatory pathways by Pathway Over-respresentation analysis upon infection. There was no significant change in gene expression that we could attribute specifically to the knockdown of TNFAIP2. Examination of the transcriptional response of A549 cells to Legionella infection with concomitant TNFAIP2 knockdown

2016-04-13 | E-GEOD-80214 | biostudies-arrayexpress

Role for TNFAIP2: Relationships with Outcomes and EMT in Urothelial Cancers under the Control of Cisplatin

Project description:Background: Cisplatin (CDDP)-based chemotherapy is the gold standard treatment for many cancer types. However, the phenotypic hallmark of tumors often changes after CDDP, with the acquisition of Epithelial-to-mesenchymal transition (EMT) and platinum resistance. Yet, the mechanisms by which cancer cells acquire EMT under the control of CDDP remain unclear. Methods: Following an investigation of urothelial cancers (UCs) before and after the acquisition of platinum resistance, we offered the new target TNFAIP2, which led to EMT and tumor invasion. TNFAIP2 expression in cancers were examined at the protein and transcription levels. Results: Clinically, up-regulated TNFAIP2 expression was identified as a significant predictor of mortality in upper urinary tract UCs. TNFAIP2 knockdown resulted in up-regulated E-cadherin expression and down-regulated TWIST expression in cancers, which decreased motile function. TNFAIP2 overexpression led to down-regulated E-cadherin expression and up-regulated TWIST expression. Clinical investigations on matched pre- and post-CDDP-treated sections confirmed up-regulated TNFAIP2 expression in CDDP-treated tumors, but down-regulated E-cadherin expression. A global gene expression analysis following TNFAIP2 knockdown identified MTDH as a positive regulator of TNFAIP2-derived EMT acquisition. Conclusions: Our results suggest a relationship between TNFAIP2 and EMT in cancers, in which MTDH expression levels in cancer cells are vital for promoting TNFAIP2-derived EMT acquisition.

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Project description:Next-generation sequencing analysis of Serpinf1(+/+) and Serpinf1(-/-) mouse calvarial osteoblast transcriptomes

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Semaphorin 3C (Sema3C) reshapes stromal microenvironment to promote hepatocellular carcinoma progression

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2024-07-10 | GSE268894 | GEO

Bcl11a (Ctip1) controls migration of cortical projection neurons through regulation of Sema3c

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WT vs c-Maf KO fetal liver macrophage

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