ReviewCell death and differentiation2024
Role of Fra-2 in cancer.
Review in Cell death and differentiation, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
23 citing papers in PubMed, 18 citations in OpenAlex.
- Single-nuclei RNA sequencing reveals obesity-associated rewiring of estrogen signaling in endometrioid adenocarcinoma.iScience · 2026Article
- Tumor-Derived LAMB3 Drives Immunosuppressive LRRC15Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- The Role of AP-1 in Cancer: Regulation, Tumor Microenvironment and Therapeutic Targeting.Biomolecules · 2026Review
- HPV8-E6 drives coordinated transcriptional and epigenetic reprogramming of keratinocytes.Tumour virus research · 2026Article
- Early radiotherapy delays acquired gefitinib resistance in EGFR-mutant NSCLC by suppressing c-FOS-associated survival signaling.Respiratory research · 2026Article
- FOSL2 drives transcriptional activation of super‑enhancer-regulatedMolecular medicine reports · 2026Article
- Fosl2 Regulates FSH-Dependent Follicle Maturation Through Feedback Amplification of FSH/FSHR Signaling.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Pulmonary fibrosis: Emerging targets and novel therapeutics.The Journal of international medical research · 2026Review
- APOE+ macrophages induce tumor cell metastatic characteristics via TNFSF12/TNFRSF12A signaling, correlating with poor patient prognosis.Cancer cell international · 2026Article
- Fra-2 controls the response to the KRAS inhibitor MRTX-1133 in pancreatic ductal adenocarcinoma.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- The histone methyltransferase NSD3 oncogene triggers ribosomal DNA transcription, interfering with FOSL2 in cancer.Cell death & disease · 2026Article
- Germacrone suppresses renal cancer growth by regulating c-Fos-mediated lipid metabolism.Lipids in health and disease · 2026Article
- Systematic analysis of functional genetic and epigenetic variants in colorectal cancer.Science advances · 2026Article
- Pan-Cancer Single-Cell RNA Sequencing Analysis Refines Multi-Origin Monocyte and Macrophage Lineages.Cancer immunology research · 2026Article
- Integrated Single-Cell and Bulk Transcriptomics Unveils Immune Profiles in Chick Erythroid Cells upon Avian PathogenicAnimals : an open access journal from MDPI · 2026Article
- UBTD1 Drives Ovarian Cancer Progression via Mutation-Associated Alterations, Stromal Microenvironment Remodeling, and TNF/AP-1 Signaling.Human mutation · 2026Article
- Circ-myh8/KAT7 Affects PANoptosis in Pulmonary Arterial Smooth Muscle Cells: Involvement of Super-Enhancers in FOSL2 Expression.Journal of the American Heart Association · 2025Article
- Proteogenomics Reveals Microproteins in Activated T Cells.Molecular & cellular proteomics : MCP · 2025Article
- Identification of IL-34 and Slc7al as potential key regulators in MASLD progression through epigenomic profiling.Epigenomics · 2025Article
- Oncofetal reprogramming drives phenotypic plasticity in WNT-dependent colorectal cancer.Nature genetics · 2025Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 3 institutions in 2 countries.
Funding
Abstract
Fos-related antigen-2 (Fra-2) is the most recently discovered member of the Fos family and, by dimerizing with Jun proteins, forms the activator protein 1 (AP-1) transcription factor. By inducing or repressing the transcription of several target genes, Fra-2 is critically involved in the modulation of cell response to a variety of extracellular stimuli, stressors and intracellular changes. In physiological conditions, Fra-2 has been found to be ubiquitously expressed in human cells, regulating differentiation and homeostasis of bone, muscle, nervous, lymphoid and other tissues. While other AP-1 members, like Jun and Fos, are well characterized, studies of Fra-2 functions in cancer are still at an early stage. Due to the lack of a trans-activating domain, which is present in other Fos proteins, it has been suggested that Fra-2 might inhibit cell transformation, eventually exerting an anti-tumor effect. In human malignancies, however, Fra-2 activity is enhanced (or induced) by dysregulation of microRNAs, oncogenes and extracellular signaling, suggesting a multifaceted role. Therefore, Fra-2 can promote or prevent transformation, proliferation, migration, epithelial-mesenchymal transition, drug resistance and metastasis formation in a tumor- and context-dependent manner. Intriguingly, recent data reports that Fra-2 is also expressed in cancer associated cells, contributing to the intricate crosstalk between neoplastic and non-neoplastic cells, that leads to the evolution and remodeling of the tumor microenvironment. In this review we summarize three decades of research on Fra-2, focusing on its oncogenic and anti-oncogenic effects in tumor progression and dissemination.
Indexed as
Identifiers
What Socratic holds
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 Socratic graph.