ArticleThe Journal of clinical investigation2023
Coordinated activation of c-Src and FOXM1 drives tumor cell proliferation and breast cancer progression.
Article in The Journal of clinical investigation, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 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
22 citing papers in PubMed, 34 citations in OpenAlex.
- The Regulatory Network of FOXM1: Orchestrating Cancer Progression and Resistance to Therapy.International journal of molecular sciences · 2026Review
- A FoxM1/Smad4 positive feedback loop promotes pancreatic cancer progression.Cell death & disease · 2026Article
- Erianin facilitates pyroptosis in endometrial cancer via targeting m6A reader YTHDF1.Chinese medicine · 2026Article
- JAK/STAT1-interferon-ISGylation networks in breast cancer resistance to inhibitors of FOXM1 and CDK4/6.NPJ breast cancer · 2026Article
- Targeting FOXM1 reshapes antitumor immunity to attenuate small cell lung cancer progression.Cancer letters · 2026Article
- Ubiquitin-specific protease 5 promotes breast cancer progression by stabilizing Forkhead box M1 through deubiquitination.CytoJournal · 2026Article
- Modelling the monstrosities: experimental and computational systems for studying polyploid giant cancer cells.Expert reviews in molecular medicine · 2025Review
- CDCP1/mitochondrial Src axis increases electron transport chain function to promote metastasis in triple-negative breast cancer.British journal of cancer · 2025Article
- Activating NEDD4L suppresses EGFR-driven lung adenocarcinoma growth via facilitating EGFR proteasomal degradation.Journal of experimental & clinical cancer research : CR · 2025Article
- Article
- Exploring Integrin α5β1 as a Potential Therapeutic Target for Pulmonary Arterial Hypertension: Insights From Comprehensive Multicenter Preclinical Studies.Circulation · 2025Article
- The Role of the Fox Gene in Breast Cancer Progression.International journal of molecular sciences · 2025Review
- FOXM1-Driven CKS1B Upregulation Promotes Pancreatic Cancer Progression and Therapeutic Resistance.International journal of biological sciences · 2025Article
- Targeting YES1 Disrupts Mitotic Fidelity and Potentiates the Response to Taxanes in Triple-Negative Breast Cancer.Cancer research · 2024Article
- Resistance to FOXM1 inhibitors in breast cancer is accompanied by impeding ferroptosis and apoptotic cell death.Breast cancer research and treatment · 2024Article
- METTL14 inhibits the proliferation, migration and invasion of prostate cancer cells by increasing m6A methylation of CDK4.Translational andrology and urology · 2024Article
- Progress and Innovative Combination Therapies in Trop-2-Targeted ADCs.Pharmaceuticals (Basel, Switzerland) · 2024Review
- NB compounds are potent and efficacious FOXM1 inhibitors in high-grade serous ovarian cancer cells.Journal of ovarian research · 2024Article
- The deubiquitinase OTUB2 promotes cervical cancer growth through stabilizing FOXM1.American journal of translational research · 2024Article
- Targeting CD24 in Cancer Immunotherapy.Biomedicines · 2023Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
19 authors at 3 institutions in 4 countries.
Funding
Abstract
Activation of the tyrosine kinase c-Src promotes breast cancer progression and poor outcomes, yet the underlying mechanisms are incompletely understood. Here, we have shown that deletion of c-Src in a genetically engineered model mimicking the luminal B molecular subtype of breast cancer abrogated the activity of forkhead box M1 (FOXM1), a master transcriptional regulator of the cell cycle. We determined that c-Src phosphorylated FOXM1 on 2 tyrosine residues to stimulate its nuclear localization and target gene expression. These included key regulators of G2/M cell-cycle progression as well as c-Src itself, forming a positive feedback loop that drove proliferation in genetically engineered and patient-derived models of luminal B-like breast cancer. Using genetic approaches and small molecules that destabilize the FOXM1 protein, we found that targeting this mechanism induced G2/M cell-cycle arrest and apoptosis, blocked tumor progression, and impaired metastasis. We identified a positive correlation between FOXM1 and c-Src expression in human breast cancer and show that the expression of FOXM1 target genes predicts poor outcomes and associates with the luminal B subtype, which responds poorly to currently approved therapies. These findings revealed a regulatory network centered on c-Src and FOXM1 that is a targetable vulnerability in aggressive luminal breast cancers.
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.