ArticleThe Journal of biological chemistry2008
FoxM1 regulates transcription of JNK1 to promote the G1/S transition and tumor cell invasiveness.
Article in The Journal of biological chemistry, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 91 papers.
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Who cites it
91 citing papers in PubMed, 146 citations in OpenAlex.
- Immunoglobulin Superfamily Protein BTNL9 Functions as a Non-Canonical Transcriptional Regulator to Suppress NSCLC Through Cell Cycle and p53 Pathways.International journal of molecular sciences · 2026Article
- A microprotein encoded by FERMT3 modulates endothelial cell protein catabolism and induces cell cycle arrest and senescence.Cell communication and signaling : CCS · 2026Article
- FOXM1 induces therapy resistance and inhibits apoptosis in a variety of human cancers.Cell death & disease · 2026Review
- SNORA58 Facilitates Radioresistance via Suppressing JNK1-Mediated Ferroptosis in Esophageal Squamous Cell Carcinoma.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Lasalocid inhibits melanoma by down-regulating FOXM1 through PI3K/AKT and JNK/P38 MAPK pathways.Journal of Cancer · 2025Article
- The conformation of FOXM1 homodimers in vivo is crucial for regulating transcriptional activities.Nucleic acids research · 2024Article
- ABL1-mediated phosphorylation promotes FOXM1-related tumorigenicity by Increasing FOXM1 stability.Cell death and differentiation · 2024Article
- Cell-Cycle-Specific Autoencoding Improves Cluster Analysis of Cycling Cardiomyocytes.Stem cells (Dayton, Ohio) · 2024Article
- Effects of lysine and methionine on mRNA expression of candidate transcription factors by primary bovine mammary epithelial cells.PloS one · 2024Article
- Invasive FoxM1 phosphorylated by PLK1 induces the polarization of tumor-associated macrophages to promote immune escape and metastasis, amplified by IFITM1.Journal of experimental & clinical cancer research : CR · 2023Article
- Inhibition of USP7 induces p53-independent tumor growth suppression in triple-negative breast cancers by destabilizing FOXM1.Cell death and differentiation · 2023Article
- Heat shock proteins and cancer: The FoxM1 connection.Biochemical pharmacology · 2023Review
- Novel insights into the multifaceted roles of mBiomarker research · 2023Review
- Foxm1 regulates cardiomyocyte proliferation in adult zebrafish after cardiac injury.Development (Cambridge, England) · 2023Article
- MiR-4521 perturbs FOXM1-mediated DNA damage response in breast cancer.Frontiers in molecular biosciences · 2023Article
- Effects of thiostrepton alone or in combination with selumetinib on triple-negative breast cancer metastasis.Molecular biology reports · 2022Article
- Chondroprotective effects of CDK4/6 inhibition via enhanced ubiquitin-dependent degradation of JUN in synovial fibroblasts.Rheumatology (Oxford, England) · 2022Article
- Integration of Adverse Outcome Pathways, Causal Networks and 'Omics to Support Chemical Hazard Assessment.Frontiers in toxicology · 2022Article
- FOXM1 is required for small cell lung cancer tumorigenesis and associated with poor clinical prognosis.Oncogene · 2021Article
- The forkhead box M1 (FOXM1) expression and antitumor effect of FOXM1 inhibition in malignant rhabdoid tumor.Journal of cancer research and clinical oncology · 2021Article
31 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
Abstract
The Forkhead box M1 (FoxM1) protein is a proliferation-specific transcription factor that plays a key role in controlling both the G(1)/S and G(2)/M transitions through the cell cycle and is essential for the development of various cancers. We show here that FoxM1 directly activates the transcription of the c-Jun N-terminal kinase (JNK1) gene in U2OS osteosarcoma cells. Expression of JNK1, which regulates the expression of genes important for the G(1)/S transition, rescues the G(1)/S but not the G(2)/M cell cycle block in FoxM1-deficient cells. Knockdown of either FoxM1 or JNK1 inhibits tumor cell migration, invasion, and anchorage-independent growth. However, expression of JNK1 in FoxM1-depleted cells does not rescue these defects, indicating that JNK1 is a necessary but insufficient downstream mediator of FoxM1 in these processes. Consistent with this interpretation, FoxM1 regulates the expression of the matrix metalloproteinases MMP-2 and MMP-9, which play a role in tumor cell invasion, through JNK1-independent and -dependent mechanisms in U2OS cells, respectively. Taken together, these findings identify JNK1 as a critical transcriptional target of FoxM1 that contributes to FoxM1-regulated cell cycle progression, tumor cell migration, invasiveness, and anchorage-independent growth.
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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.