ArticleMolecular biology of the cell2008
Disruption of c-Jun reduces cellular migration and invasion through inhibition of c-Src and hyperactivation of ROCK II kinase.
Article in Molecular biology of the cell, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 33 citations in OpenAlex.
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- The Renaissance of CDK Inhibitors in Breast Cancer Therapy: An Update on Clinical Trials and Therapy Resistance.Cancers · 2022Review
- The membrane-associated form of cyclin D1 enhances cellular invasion.Oncogenesis · 2020Article
- Endogenous Cyclin D1 Promotes the Rate of Onset and Magnitude of Mitogenic Signaling via Akt1 Ser473 Phosphorylation.Cell reports · 2020Article
- Understanding Transcriptional Networks Regulating Initiation of Cutaneous Wound Healing.The Yale journal of biology and medicine · 2020Review
- The peroxidase PRDX1 inhibits the activated phenotype in mammary fibroblasts through regulating c-Jun N-terminal kinases.BMC cancer · 2019Article
- Dachshund Depletion Disrupts Mammary Gland Development and Diverts the Composition of the Mammary Gland Progenitor Pool.Stem cell reports · 2019Article
- Biological Function of Ribosomal Protein L10 on Cell Behavior in Human Epithelial Ovarian Cancer.Journal of Cancer · 2018Article
- c-Jun enhances intestinal epithelial restitution after wounding by increasing phospholipase C-γ1 transcription.American journal of physiology. Cell physiology · 2017Article
- Short term exposure of beta cells to low concentrations of interleukin-1β improves insulin secretion through focal adhesion and actin remodeling and regulation of gene expression.The Journal of biological chemistry · 2015Article
- Article
- An emerging role for long non-coding RNAs in cancer metastasis.Frontiers in genetics · 2014Review
- c-Jun induces mammary epithelial cellular invasion and breast cancer stem cell expansion.The Journal of biological chemistry · 2010Article
Corrections and comments
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Authors and funding
14 authors at 5 institutions in 3 countries.
Funding
Abstract
The spread of metastatic tumors to different organs is associated with poor prognosis. The metastatic process requires migration and cellular invasion. The protooncogene c-jun encodes the founding member of the activator protein-1 family and is required for cellular proliferation and DNA synthesis in response to oncogenic signals and plays an essential role in chemical carcinogenesis. The role of c-Jun in cellular invasion remains to be defined. Genetic deletion of c-Jun in transgenic mice is embryonic lethal; therefore, transgenic mice encoding a c-Jun gene flanked by LoxP sites (c-jun(f/f)) were used. c-jun gene deletion reduced c-Src expression, hyperactivated ROCK II signaling, and reduced cellular polarity, migration, and invasiveness. c-Jun increased c-Src mRNA abundance and c-Src promoter activity involving an AP-1 site in the c-Src promoter. Transduction of c-jun(-/-) cells with either c-Jun or c-Src retroviral expression systems restored the defective cellular migration of c-jun(-/-) cells. As c-Src is a critical component of pathways regulating proliferation, survival, and metastasis, the induction of c-Src abundance, by c-Jun, provides a novel mechanism of cooperative signaling in cellular invasion.
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Registered trials
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