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

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

ORGANISM(S): Homo sapiens

PROVIDER: GSE57529 | GEO | 2014/06/30

SECONDARY ACCESSION(S): PRJNA246601

REPOSITORIES: GEO

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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

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

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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).

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