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C-Jun promotes cell migration and drives expression of the motility factor ENPP2 in soft tissue sarcomas [RNA-Seq]

ABSTRACT: We assayed the effect of c-Jun overexpression on gene expression in the three DDLPS cell lines using RNA-Seq (Illumina).

ORGANISM(S): Homo sapiens

PROVIDER: GSE57530 | GEO | 2014/06/30

SECONDARY ACCESSION(S): PRJNA246600

REPOSITORIES: GEO

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c-Jun promotes cell migration and drives expression of the motility factor ENPP2 in soft tissue sarcomas [RNA-Seq]

Project description:We assayed the effect of c-Jun overexpression on gene expression in the three DDLPS cell lines using RNA-Seq (Illumina). 141, LPS12 and 510 has been overexpressed with c-Jun or control c-DNA and results were analyzed in high-througput sequencing metadata.

2014-06-30 | E-GEOD-57530 | biostudies-arrayexpress

c-Jun promotes cell migration and drives expression of the motility factor ENPP2 in soft tissue sarcomas [array]

Project description:Affymetrix exon arrays to identify genes that were differentially expressed after c-Jun inhibition in LPS cell line with and with no Jun amplification. We compared the consequences of c-Jun inhibition in LP6 (genomically c-Jun amplified) and LPS141 (non-amplified) DDLPS cells after Lentivrus modulation. We used lentivirus to deliver 2 control (shGFP, shNT) and 2 Jun (shJun1, shJun3) shRNAs and harvested total RNA on days 4 and 7 after infection, timepoints at which we observed maximum c-Jun inhibition by qRT-PCR and immunoblotting

2014-06-30 | E-GEOD-57529 | biostudies-arrayexpress

c-Jun promotes cell migration and drives expression of the motility factor ENPP2 in soft tissue sarcomas [array]

Project description:Affymetrix exon arrays to identify genes that were differentially expressed after c-Jun inhibition in LPS cell line with and with no Jun amplification.

2014-06-30 | GSE57529 | GEO

c-Jun promotes cell migration and drives expression of the motility factor ENPP2 in soft tissue sarcomas.

Project description:Genomic amplification of the c-Jun proto-oncogene has been identified in ?30% of dedifferentiated liposarcomas (DDLPS), but the functional contribution of c-Jun to the progression of DDLPS remains poorly understood. In previous work we showed that knock-down of c-Jun by RNA interference impaired the in vitro proliferation and in vivo growth of a DDLPS cell line (LP6) with genomic amplification of the c-Jun locus. Here, we used gene expression analysis and functional studies in a broad panel of cell lines to further define the role of c-Jun in DDLPS and other soft tissue sarcomas. We show that c-Jun knock-down impairs transition through the G1 phase of the cell cycle in multiple DDLPS cell lines. We also found that high levels of c-Jun expression are both necessary and sufficient to promote DDLPS cell migration and invasion in vitro. Our data suggest that high levels of c-Jun enhance motility in part by driving the expression of ENPP2/Autotaxin. c-Jun over-expression has minimal effects on in vitro proliferation but substantially enhances the in vivo growth of weakly tumourigenic DDLPS cell lines. Finally, we provide evidence that c-Jun genomic amplification and over-expression may have similar functional consequences in other types of soft tissue sarcoma. Our data suggest a model in which relatively low levels of c-Jun are sufficient for in vitro proliferation, but high levels of c-Jun enhance invasiveness and capacity for in vivo tumour growth. These observations provide an explanation for the selective advantage provided by c-Jun genomic amplification in vivo and suggest that sarcomas with elevated c-Jun levels are likely to have a particularly high malignant potential. Data from exon array and RNA-Seq experiments have been deposited in the GEO database (Accession No. GSE57531).

| S-EPMC4472460 | biostudies-literature

c-Jun promotes cell migration and drives expression of the motility factor ENPP2 in soft tissue sarcomas

Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

2014-06-30 | E-GEOD-57531 | biostudies-arrayexpress

c-Jun promotes cell migration and drives expression of the motility factor ENPP2 in soft tissue sarcomas

Project description:This SuperSeries is composed of the SubSeries listed below.

2014-06-30 | GSE57531 | GEO

ERK signaling regulates opposing functions of JUN family transcription factors in prostate cancer cell migration

Project description:Knockdowns of c-JUN and JUND had opposite effects on PC3 prostate cell migration. We predicted that c-JUN and JUND control the same set of cell migration genes, but in opposite directions. To test this hypothesis, mRNA with expression changes in c-JUN and JUND knockdown PC3 cell lines were compared to mRNA levels in control (luciferase knockdown) PC3 cells by RNA-seq. mRNA profiles of luciferase knockdown (WT), c-Jun knockdown, and Jun-D knockdown in PC3 cells were generated using deep sequencing, in triplicate, using Illumina HiSeq. Knockdowns were stable shRNA expression from a lentiviral construct selected with puromycin.

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Genome-wide maps of H3K27ac, H3K4me1, JUN and p-JUN in JUN overexpressed or JUN inactivated fibroblasts

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JUN promotes hypertrophic skin scarring via CD36

Project description:Hypertrophic skin scarring following dermal injury causes extreme pain and psychological trauma for patients. Unfortuately, we do not have effective treatments to prevent or reverse skin scarring. Using RNA and ATAC sequencing of mouse and human fibroblasts, we show that JUN expressing fibroblasts are responsible for skin scarring by regulating CD36 expression. In summary, we show that CD36 antagonism by represent a therapeutic target to overcome JUN hypertrophic skin scarring.

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ERK signaling regulates opposing functions of JUN family transcription factors in prostate cancer cell migration

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