Transcriptional control of SPARC by v-Jun and other members of the AP1 family of transcription factors

Vial, Emmanuel; Perez, Sandrine; Castellazzi, Marc

doi:10.1038/sj.onc.1203867

Cited by 31 publications

(23 citation statements)

References 41 publications

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“…12 In fibroblasts, TNF promotes TGF-␤1 expression via AP-1 activation, 48 which also controls SPARC expression. 49 The similarity between SPARC and TGF-␤1 suggests their dual effect on leukocyte and fibroblasts, reducing inflammation and promoting fibrogenesis, respectively.…”

Section: Discussionmentioning

confidence: 99%

SPARC Oppositely Regulates Inflammation and Fibrosis in Bleomycin-Induced Lung Damage

Sangaletti

Tripodo

Cappetti

et al. 2011

The American Journal of Pathology

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Section: Discussionmentioning

confidence: 99%

SPARC Oppositely Regulates Inflammation and Fibrosis in Bleomycin-Induced Lung Damage

Sangaletti

Tripodo

Cappetti

et al. 2011

The American Journal of Pathology

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“…In the case of the murine interleukin-4 gene, for example, the apparent AP-1-responsive region is unrelated to the AP-1 consensus sequence (Rooney et al, 1995). Atypical AP-1-responsive gene elements that may accommodate a number of alternate bZIP factors have also been found in the osteocalcin and secreted protein acidic and rich in cysteine genes, among others (Vial et al, 2000;Akhouayri and St-Arnaud, 2007). In the present study, transient transfection and EMSA analysis were used to identify the Ϫ105/Ϫ88-base pair region of the CYP2J2 gene 5Ј-flank as an atypical bZIP binding sequence that was responsive to c-Jun/Nrf2 dimers.…”

Section: Discussionmentioning

confidence: 99%

Up-Regulation of Human CYP2J2 in HepG2 Cells by Butylated Hydroxyanisole Is Mediated by c-Jun and Nrf2

Lee

Murray²

2010

Molecular Pharmacology

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“…Of the AP-1-regulated genes identified thus far, four have been reported to induce a change in cellular phenotype (Hartl et al, 2001;Vogt, 2001). Two v-jun upregulated genes in CEF, HB-EGF and JAC causes partial transformation (Fu et al, 1999; Hartl et al, 2001), while reintroduction of v-jun downregulated genes, SPARC and SSeCKS, result in partial reversion of vJun-induced transformation (Cohen et al, 2001;Vial et al, 2000). In contrast to vJun regulation in CEFs, SPARC is upregulated in cJun-overexpressing MCF7 cells and it has been associated with motility and invasion of these cells (Briggs et al, 2002).…”

Section: Discussionmentioning

confidence: 99%

AP-1 complexes containing cJun and JunB cause cellular transformation of Rat1a fibroblasts and share transcriptional targets

2003

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To investigate the role of individual Jun proteins in cell growth and transformation, we have used a doxycyclineinducible retroviral vector to regulate their expression in rat fibroblasts. AP-1 complexes enriched with cJun and JunB result in morphological alterations and anchorageindependent cell growth consistent with a transformationlike phenotype, whereas complexes enriched with JunD had an antiproliferative effect. These results suggest that genes regulated by both cJun and JunB are potentially involved in transformation and that they can be distinguished from those regulated by AP-1 complexes containing JunD. To identify genes regulated by cJun and JunB that may have a role in anchorage-independent growth, we investigated differential gene expression by each of the Jun family members using the Affymetrix Rat oligonucleotide microarray, RG_U34A containing approximately 8000 genes. Differentially regulated genes were identified and grouped for correlation with regulation by the different Jun proteins. A total of 33 candidate genes were found to be differentially regulated by both cJun and JunB and not by JunD. These genes have roles in cell metabolism, growth, signal transduction, migration and adhesion. We validated the differential regulation by cJun and JunB of 10 candidate genes by Northern blot analysis. Of these, eight were further characterized as potential direct targets of AP-1 regulation based on Northern blot results showing differential regulation that correlate with cJun expression. Our results show that inducible cJun and JunB expression result in anchorage-independent growth of Rat1a cells, distinct from JunD-expressing cells. This model system and a functional genomic approach enabled us to differentiate AP-1-regulated genes involved in transformation from AP-1-regulated genes known as bystander genes. This approach significantly reduces the number of bystanders and allows for the targeting of genes specifically involved in transformation.

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Transcriptional control of SPARC by v-Jun and other members of the AP1 family of transcription factors

Cited by 31 publications

References 41 publications

SPARC Oppositely Regulates Inflammation and Fibrosis in Bleomycin-Induced Lung Damage

SPARC Oppositely Regulates Inflammation and Fibrosis in Bleomycin-Induced Lung Damage

Up-Regulation of Human CYP2J2 in HepG2 Cells by Butylated Hydroxyanisole Is Mediated by c-Jun and Nrf2

AP-1 complexes containing cJun and JunB cause cellular transformation of Rat1a fibroblasts and share transcriptional targets

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