ArticleGenome biology2015
FOXM1 binds directly to non-consensus sequences in the human genome.
Article in Genome biology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 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
45 citing papers in PubMed, 66 citations in OpenAlex.
- Single-cell analysis identifies TOP2α as a critical regulator of G2/M entry and differentiation-dependent productive HPV replication.bioRxiv : the preprint server for biology · 2026Article
- FOXM1 induces therapy resistance and inhibits apoptosis in a variety of human cancers.Cell death & disease · 2026Review
- FOXM1 as a candidate dosage rheostat and state selector in breast cancer: linking multilevel regulation to adaptive plasticity and therapy resistance.Frontiers in oncology · 2026Review
- Integrated Network Analysis Reveals a Directly Regulatory Network of FOXM1 Associated With the Cell Cycle in Lung Adenocarcinoma.Bioinformatics and biology insights · 2026Article
- A positive feedback loop between KPNA2 and FOXM1 promotes the proliferation of lung adenocarcinoma.European journal of medical research · 2025Article
- Stochastic variation in the FOXM1 transcription program mediates replication stress tolerance.Molecular oncology · 2025Article
- CD133Heliyon · 2024Article
- Unravelling the therapeutic potential of forkhead box proteins in breast cancer: An update (Review).Oncology reports · 2024Review
- NB compounds are potent and efficacious FOXM1 inhibitors in high-grade serous ovarian cancer cells.Journal of ovarian research · 2024Article
- Article
- The role of FoxM1 in immune cells.Clinical and experimental medicine · 2023Review
- Noncanonical binding of transcription factors: time to revisitMolecular biology of the cell · 2023Review
- MRPL51 is a downstream target of FOXM1 in promoting the malignant behaviors of lung adenocarcinoma.Oncology letters · 2023Article
- RNF112-mediated FOXM1 ubiquitination suppresses the proliferation and invasion of gastric cancer.JCI insight · 2023Article
- FOXM1: Functional Roles of FOXM1 in Non-Malignant Diseases.Biomolecules · 2023Review
- Coordinated activation of c-Src and FOXM1 drives tumor cell proliferation and breast cancer progression.The Journal of clinical investigation · 2023Article
- Estrogen regulates divergent transcriptional and epigenetic cell states in breast cancer.Nucleic acids research · 2022Article
- Structure and function of MuvB complexes.Oncogene · 2022Review
- The human ion channel TRPM2 modulates cell survival in neuroblastoma through E2F1 and FOXM1.Scientific reports · 2022Article
- E2F2 promotes lung adenocarcinoma progression through B-Myb- and FOXM1-facilitated core transcription regulatory circuitry.International journal of biological sciences · 2022Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundThe Forkhead (FKH) transcription factor FOXM1 is a key regulator of the cell cycle and is overexpressed in most types of cancer. FOXM1, similar to other FKH factors, binds to a canonical FKH motif in vitro. However, genome-wide mapping studies in different cell lines have shown a lack of enrichment of the FKH motif, suggesting an alternative mode of chromatin recruitment. We have investigated the role of direct versus indirect DNA binding in FOXM1 recruitment by performing ChIP-seq with wild-type and DNA binding deficient FOXM1.
resultsAn in vitro fluorescence polarization assay identified point mutations in the DNA binding domain of FOXM1 that inhibit binding to a FKH consensus sequence. Cell lines expressing either wild-type or DNA binding deficient GFP-tagged FOXM1 were used for genome-wide mapping studies comparing the distribution of the DNA binding deficient protein to the wild-type. This shows that interaction of the FOXM1 DNA binding domain with target DNA is essential for recruitment. Moreover, analysis of the protein interactome of wild-type versus DNA binding deficient FOXM1 shows that the reduced recruitment is not due to inhibition of protein-protein interactions.
conclusionsA functional DNA binding domain is essential for FOXM1 chromatin recruitment. Even in FOXM1 mutants with almost complete loss of binding, the protein-protein interactions and pattern of phosphorylation are largely unaffected. These results strongly support a model whereby FOXM1 is specifically recruited to chromatin through co-factor interactions by binding directly to non-canonical DNA sequences.
Indexed as
Identifiers
What OpenQuestion 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 OpenQuestion graph.