ArticleOncogene2002
Transcriptional upregulation of SPARC, in response to c-Jun overexpression, contributes to increased motility and invasion of MCF7 breast cancer cells.
Article in Oncogene, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers.
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Who cites it
52 citing papers in PubMed, 114 citations in OpenAlex.
- Regulatory Mechanisms of SPARC Overexpression in Melanoma Progression.International journal of molecular sciences · 2025Article
- HDAC10 inhibition represses melanoma cell growth and BRAF inhibitor resistance via upregulating SPARC expression.NAR cancer · 2024Article
- Diosgenin restores memory function via SPARC-driven axonal growth from the hippocampus to the PFC in Alzheimer's disease model mice.Molecular psychiatry · 2023Article
- SPARC in cancer-associated fibroblasts is an independent poor prognostic factor in non-metastatic triple-negative breast cancer and exhibits pro-tumor activity.International journal of cancer · 2023Article
- Article
- Targeted co-delivery biomimetic nanoparticles reverse macrophage polarization for enhanced rheumatoid arthritis therapy.Drug delivery · 2022Article
- Growth hormone/IGF-I-dependent signaling restores decreased expression of the myokine SPARC in aged skeletal muscle.Journal of molecular medicine (Berlin, Germany) · 2022Article
- Transcription factor Runx2 changes the expression of some matricellular proteins in metastatic breast cancer cells.Molecular biology reports · 2022Article
- A Network Pharmacology Study on the Molecular Mechanisms of FDY003 for Breast Cancer Treatment.Evidence-based complementary and alternative medicine : eCAM · 2021Article
- MiR-29c-3p inhibits epithelial-mesenchymal transition to inhibit the proliferation, invasion and metastasis of cervical cancer cells by targeting SPARC.Annals of translational medicine · 2021Article
- A 9-kDa matricellular SPARC fragment released by cathepsin D exhibits pro-tumor activity in the triple-negative breast cancer microenvironment.Theranostics · 2021Article
- Biochemical Predictors of Response to Neoadjuvant Therapy in Pancreatic Ductal Adenocarcinoma.Frontiers in oncology · 2020Review
- Fangchinoline, a Bisbenzylisoquinoline Alkaloid can Modulate Cytokine-Impelled Apoptosis via the Dual Regulation of NF-κB and AP-1 Pathways.Molecules (Basel, Switzerland) · 2019Article
- Association of SPARC gene polymorphisms rs3210714 and rs7719521 with VEGF expression and utility of Nottingham Prognostic Index scoring in breast cancer in a sample of Egyptian women.Molecular biology reports · 2018Article
- Elimination of classically-activated macrophages in tumor-conditioned medium by alternatively-activated macrophages.Biology open · 2017Article
- Expression levels of transcription factors c-Fos and c-Jun and transmembrane protein HAb18G/CD147 in urothelial carcinoma of the bladder.Molecular medicine reports · 2017Article
- Efficacy and safety of weekly intravenous nanoparticle albumin-bound paclitaxel for non-small cell lung cancer patients who have failed at least two prior systemic treatments.Thoracic cancer · 2017Article
- SPARC Promotes Cell Invasion In Vivo by Decreasing Type IV Collagen Levels in the Basement Membrane.PLoS genetics · 2016Article
- Peritumoral SPARC expression and patient outcome with resectable intrahepatic cholangiocarcinoma.OncoTargets and therapy · 2015Article
- SPARC mediates metastatic cooperation between CSC and non-CSC prostate cancer cell subpopulations.Molecular cancer · 2014Article
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 2 countries.
Funding
Abstract
Overexpression of the c-Jun proto-oncogene in MCF7 breast cancer cells results in a variety of phenotype changes related to malignant progression including increased motility and invasion. Concurrent with these phenotypic effects are changes in the expression of multiple gene targets. We previously demonstrated that expression of the SPARC/osteonectin gene, while undetectable in the MCF7 cell line, is highly induced in response to stable c-Jun overexpression (c-Jun/MCF7). Because the SPARC gene product is associated with tumor cell invasion in a variety of different cancers, we have examined its role in mediating the phenotypic changes induced by c-Jun in MCF7 cells. We found that antisense mediated suppression of SPARC dramatically inhibits both motility and invasion in this c-Jun/MCF7 model. In contrast, stable overexpression of SPARC in the parental MCF7 cell line is not sufficient to stimulate cell motility or invasion. Examination of the promoter region of the human SPARC gene reveals three non-canonical AP-1 sites. We demonstrate that one of these sites binds c-Jun/Fra1 heterodimers in vitro, but that this and the other AP-1 like sites are dispensable with respect to c-Jun stimulated SPARC promoter activation. Deletion analysis identified a region between -120 and -70 as a c-Jun responsive element sufficient to induce maximal promoter activation. This region does not contain any AP-1 sites but does mediate binding by SP1 'like' complexes. Furthermore, this region is necessary for SP1/SP3 responsiveness in Drosophila SL2 cells. These results demonstrate that SPARC plays an important role in stimulating motility and the invasive behavior of c-Jun/MCF7 cells and that SPARC promoter activation by c-Jun appears to occur through an indirect mechanism.
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Registered trials
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.