ArticleOncogene2005
cFos is critical for MCF-7 breast cancer cell growth.
Article in Oncogene, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers, 1 of them a synthesis that pooled it.
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Who cites it
40 citing papers in PubMed, 1 synthesis or guideline pooled it, 75 citations in OpenAlex.
- Prognostic role of EGR1 in breast cancer: a systematic review.BMB reports · 2021Pooled it
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- The Discovery of Small ERK5 Inhibitors via Structure-Based Virtual Screening, Biological Evaluation and MD Simulations.Molecules (Basel, Switzerland) · 2025Article
- Ebselen Suppresses Breast Cancer Tumorigenesis by Inhibiting YTHDF1-Mediated c-Fos Expression.International journal of molecular sciences · 2025Article
- BC-predict: mining of signal biomarkers and production of models for early-stage breast cancer subtyping and prognosis.Frontiers in bioinformatics · 2025Article
- Dysregulated gene subnetworks in breast invasive carcinoma reveal novel tumor suppressor genes.Scientific reports · 2024Article
- Expression and Functional Analysis of Immuno-Micro-RNAs mir-146a and mir-326 in Colorectal Cancer.Current issues in molecular biology · 2024Article
- Modulation of ERK5 Activity as a Therapeutic Anti-Cancer Strategy.Journal of medicinal chemistry · 2023Review
- Distinct biogenesis pathways may have led to functional divergence of the human and Drosophila Arglu1 sisRNA.EMBO reports · 2023Article
- Protection of c-Fos from autophagic degradation by PRMT1-mediated methylation fosters gastric tumorigenesis.International journal of biological sciences · 2023Article
- The Interplay of GPER1 with 17β-Aminoestrogens in the Regulation of the Proliferation of Cervical and Breast Cancer Cells: A Pharmacological Approach.International journal of environmental research and public health · 2022Article
- Suppression of the malignancy of mammary tumor in mice model by inactivated preparation ofVeterinary research forum : an international quarterly journal · 2022Article
- Epigenetic alterations at distal enhancers are linked to proliferation in human breast cancer.NAR cancer · 2022Article
- Hyperactivation of MAPK Induces Tamoxifen Resistance in SPRED2-Deficient ERα-Positive Breast Cancer.Cancers · 2022Article
- Reduced RBPMS Levels Promote Cell Proliferation and Decrease Cisplatin Sensitivity in Ovarian Cancer Cells.International journal of molecular sciences · 2022Article
- High-Intensity Aerobic Exercise Suppresses Cancer Growth by Regulating Skeletal Muscle-Derived Oncogenes and Tumor Suppressors.Frontiers in molecular biosciences · 2022Article
- The Adipokine Component in the Molecular Regulation of Cancer Cell Survival, Proliferation and Metastasis.Pathology oncology research : POR · 2021Review
- Selective antagonism of cJun for cancer therapy.Journal of experimental & clinical cancer research : CR · 2020Review
- Article
- Activation of Oncogenic Super-Enhancers Is Coupled with DNA Repair by RAD51.Cell reports · 2019Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The activating protein-1 (AP-1) transcription factor is a converging point of multiple signal transduction pathways in many cells. We have previously demonstrated that overexpressing Tam67, a dominant-negative (DN) form of cJun, blocks AP-1 activity and inhibits breast cancer cell growth. We hypothesized that Tam67 forms dimers with other AP-1 proteins to suppress the growth of breast cancer cells. In the present study, we used immunoprecipitation-Western blotting to demonstrate that Tam67 binds all Jun and Fos proteins in breast cancer cells. In addition, we used two variants of the Tam67 mutant to investigate whether Jun or Fos protein was required for breast cancer cell growth. We created a Tam/Fos mutant in which the cJun dimerization domain was replaced by the cFos dimerization domain, and a Tam/Squelcher mutant in which the cJun dimerization domain was deleted. We then isolated MCF-7 cell lines that stably expressed these cJun-DN mutants under the control of an inducible promoter. Using AP-1-dependent reporter assays, we observed that Tam67 and Tam/Fos mutants inhibited AP-1 transcriptional activity, while the Tam/Squelcher mutant did not. We then determined whether Tam/Fos or Tam/Squelcher inhibited breast cell growth as well as Tam67. We found that while Tam67 repressed cell growth, neither Tam/Fos nor Tam/Squelcher mutant affected cell growth. These results indicate that Tam67 likely inactivates Fos family member proteins to suppress breast cancer cell growth. Finally, we performed antisense experiments to knock down the expression of individual family members (cJun or cFos). Our results demonstrated that antisense cFos inhibited breast cancer cell proliferation and colony formation, while antisense cJun did not. These results suggest that Tam67 suppresses breast cancer cell growth by interacting with Fos family members, specifically with cFos, to produce an inactive AP-1 complex.
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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.