ArticleThe Journal of pathology2014
c-Jun promotes cell migration and drives expression of the motility factor ENPP2 in soft tissue sarcomas.
Article in The Journal of pathology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 37 citations in OpenAlex.
- Phase 2 study of palbociclib plus retifanlimab in patients with advanced dedifferentiated liposarcoma.Journal for immunotherapy of cancer · 2026Trial
- Jun, an Oncological Foe or Friend?International journal of molecular sciences · 2025Review
- ENPP2 promotes progression and lipid accumulation via AMPK/SREBP1/FAS pathway in chronic lymphocytic leukemia.Cellular & molecular biology letters · 2024Article
- Autotaxin-Lysophosphatidate Axis: Promoter of Cancer Development and Possible Therapeutic Implications.International journal of molecular sciences · 2024Review
- Article
- E2F7 drives autotaxin/Enpp2 transcription via chromosome looping: Repression by p53 in murine but not in human carcinomas.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2023Article
- Review
- Endocrine resistance and breast cancer plasticity are controlled by CoREST.Nature structural & molecular biology · 2022Article
- C-Myc Expression in Oral Squamous Cell Carcinoma: Molecular Mechanisms in Cell Survival and Cancer Progression.Pharmaceuticals (Basel, Switzerland) · 2022Article
- Article
- Review
- Update on genomic and molecular landscapes of well-differentiated liposarcoma and dedifferentiated liposarcoma.Molecular biology reports · 2021Review
- Dysregulation of lysophospholipid signaling by p53 in malignant cells and the tumor microenvironment.Cellular signalling · 2021Review
- Involvement of autotaxin in the pathophysiology of elevated intraocular pressure in Posner-Schlossman syndrome.Scientific reports · 2020Article
- c-Jun Overexpression Accelerates Wound Healing in Diabetic Rats by Human Umbilical Cord-Derived Mesenchymal Stem Cells.Stem cells international · 2020Article
- The peroxidase PRDX1 inhibits the activated phenotype in mammary fibroblasts through regulating c-Jun N-terminal kinases.BMC cancer · 2019Article
- The PTEN Tumor Suppressor Gene in Soft Tissue Sarcoma.Cancers · 2019Review
- Understanding Keloid Pathobiology From a Quasi-Neoplastic Perspective: Less of a Scar and More of a Chronic Inflammatory Disease With Cancer-Like Tendencies.Frontiers in immunology · 2019Review
- Schwann Cell-Like Cells Derived from Human Amniotic Mesenchymal Stem Cells Promote Peripheral Nerve Regeneration through a MicroRNA-214/c-Jun Pathway.Stem cells international · 2019Article
- Autotaxin in Pathophysiology and Pulmonary Fibrosis.Frontiers in medicine · 2018Review
Corrections and comments
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Authors and funding
10 authors at 5 institutions in 1 country.
Funding
Abstract
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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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.