HCSGD entry for FOXM1
1. General information
| Official gene symbol | FOXM1 |
|---|---|
| Entrez ID | 2305 |
| Gene full name | forkhead box M1 |
| Other gene symbols | FKHL16 FOXM1B HFH-11 HFH11 HNF-3 INS-1 MPHOSPH2 MPP-2 MPP2 PIG29 TGT3 TRIDENT |
| Links to Entrez Gene | Links to Entrez Gene |
2. Neighbors in the network
3. Gene ontology annotation
GO ID | GO term | Evidence | Category |
|---|---|---|---|
| GO:0000086 | G2/M transition of mitotic cell cycle | IDA | biological_process |
| GO:0000122 | Negative regulation of transcription from RNA polymerase II promoter | IMP | biological_process |
| GO:0001558 | Regulation of cell growth | TAS | biological_process |
| GO:0001570 | Vasculogenesis | IBA | biological_process |
| GO:0001889 | Liver development | IBA | biological_process |
| GO:0003677 | DNA binding | IDA TAS | molecular_function |
| GO:0003690 | Double-stranded DNA binding | IBA | molecular_function |
| GO:0003700 | Sequence-specific DNA binding transcription factor activity | IDA IEA TAS | molecular_function |
| GO:0003705 | RNA polymerase II distal enhancer sequence-specific DNA binding transcription factor activity | IBA | molecular_function |
| GO:0005515 | Protein binding | IPI | molecular_function |
| GO:0005634 | Nucleus | IDA | cellular_component |
| GO:0005667 | Transcription factor complex | IBA | cellular_component |
| GO:0005730 | Nucleolus | IDA | cellular_component |
| GO:0005737 | Cytoplasm | IDA | cellular_component |
| GO:0006281 | DNA repair | IEA | biological_process |
| GO:0006355 | Regulation of transcription, DNA-templated | IDA TAS | biological_process |
| GO:0006366 | Transcription from RNA polymerase II promoter | IBA IDA | biological_process |
| GO:0006978 | DNA damage response, signal transduction by p53 class mediator resulting in transcription of p21 class mediator | IMP | biological_process |
| GO:0007049 | Cell cycle | TAS | biological_process |
| GO:0007389 | Pattern specification process | IBA | biological_process |
| GO:0008134 | Transcription factor binding | IBA | molecular_function |
| GO:0008284 | Positive regulation of cell proliferation | IMP | biological_process |
| GO:0008301 | DNA binding, bending | IBA | molecular_function |
| GO:0009790 | Embryo development | IBA | biological_process |
| GO:0009888 | Tissue development | IBA | biological_process |
| GO:0019901 | Protein kinase binding | IPI | molecular_function |
| GO:0032873 | Negative regulation of stress-activated MAPK cascade | IMP | biological_process |
| GO:0042127 | Regulation of cell proliferation | NAS | biological_process |
| GO:0043565 | Sequence-specific DNA binding | IEA | molecular_function |
| GO:0044212 | Transcription regulatory region DNA binding | IEA | molecular_function |
| GO:0045892 | Negative regulation of transcription, DNA-templated | IMP | biological_process |
| GO:0045893 | Positive regulation of transcription, DNA-templated | IMP | biological_process |
| GO:0045944 | Positive regulation of transcription from RNA polymerase II promoter | IDA IMP | biological_process |
| GO:0046578 | Regulation of Ras protein signal transduction | IMP | biological_process |
| GO:0051090 | Regulation of sequence-specific DNA binding transcription factor activity | IBA | biological_process |
| GO:0071156 | Regulation of cell cycle arrest | IMP | biological_process |
| GO:0090344 | Negative regulation of cell aging | IMP | biological_process |
| GO:2000377 | Regulation of reactive oxygen species metabolic process | IMP | biological_process |
| GO:2000781 | Positive regulation of double-strand break repair | IMP | biological_process |
| GO:2001141 | Regulation of RNA biosynthetic process | IDA TAS | biological_process |
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4. Expression levels in datasets
- Meta-analysis result
| p-value up | p-value down | FDR up | FDR down |
|---|---|---|---|
| 0.9773757608 | 0.0000138787 | 0.9999902473 | 0.0071627451 |
- Individual experiment result
( "-" represent NA in the specific microarray platform )
( "-" represent NA in the specific microarray platform )
| Data source | Up or down | Log fold change |
|---|---|---|
| GSE11954 | Down | -0.9398659996 |
| GSE13712_SHEAR | Down | -0.5073770244 |
| GSE13712_STATIC | Down | -1.0073222923 |
| GSE19018 | Up | 0.0401548622 |
| GSE19899_A1 | Down | -1.0764283518 |
| GSE19899_A2 | Down | -4.6403049718 |
| PubMed_21979375_A1 | Down | -4.0685096903 |
| PubMed_21979375_A2 | Down | -4.5358402000 |
| GSE35957 | Down | -3.6372346882 |
| GSE36640 | Down | -4.5744709950 |
| GSE54402 | Down | -0.8527302827 |
| GSE9593 | Down | -1.5539458208 |
| GSE43922 | Down | -2.5505653743 |
| GSE24585 | Down | -0.0861646744 |
| GSE37065 | Down | -1.3743563379 |
| GSE28863_A1 | Down | -0.0746853586 |
| GSE28863_A2 | Up | 0.7162397302 |
| GSE28863_A3 | Down | -0.1065589492 |
| GSE28863_A4 | Up | 0.1999581241 |
| GSE48662 | Down | -1.4475837028 |
5. Regulation relationships with compounds/drugs/microRNAs
- Compounds
Not regulated by compounds
- Drugs
Not regulated by drugs
- MicroRNAs
- mirTarBase
- mirTarBase
MiRNA_name | mirBase ID | miRTarBase ID | Experiment | Support type | References (Pubmed ID) |
|---|---|---|---|---|---|
| hsa-miR-134-5p | MIMAT0000447 | MIRT006979 | Luciferase reporter assay//Western blot | Functional MTI | 23010597 |
| hsa-miR-26b-5p | MIMAT0000083 | MIRT030070 | Microarray | Functional MTI (Weak) | 19088304 |
| hsa-miR-186-5p | MIMAT0000456 | MIRT045084 | CLASH | Functional MTI (Weak) | 23622248 |
| hsa-miR-149-5p | MIMAT0000450 | MIRT052645 | Luciferase reporter assay//Western blot | Functional MTI | 23762558 |
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- mirRecord
No target information from mirRecord
- mirRecord
6. Text-mining results about the gene
Gene occurances in abstracts of cellular senescence-associated articles: 15 abstracts the gene occurs.
PubMed ID of the article | Sentenece the gene occurs |
|---|---|
| 26236688 | The differential molecular profiles between MOE(HIGH) and MOE(LOW) were determined using RNA-Seq and confirmed by protein expression to uncover pathways important in transformation, like the p53 pathway, the FOXM1 pathway, WNT signaling, and splicing |
| 26236688 | MOE(HIGH) had enhanced protein expression of c-myc, Cyclin E, p53, and FOXM1 with reduced expression of p21 |
| 25961928 | Paclitaxel targets FOXM1 to regulate KIF20A in mitotic catastrophe and breast cancer paclitaxel resistance |
| 25961928 | FOXM1 has been implicated in taxane resistance, but the molecular mechanism involved remains elusive |
| 25961928 | In here, we show that FOXM1 depletion can sensitize breast cancer cells and mouse embryonic fibroblasts into entering paclitaxel-induced senescence, with the loss of clonogenic ability, and the induction of senescence-associated beta-galactosidase activity and flat cell morphology |
| 25961928 | We also demonstrate that FOXM1 regulates the expression of the microtubulin-associated kinesin KIF20A at the transcriptional level directly through a Forkhead response element (FHRE) in its promoter |
| 25961928 | Similar to FOXM1, KIF20A expression is downregulated by paclitaxel in the sensitive MCF-7 breast cancer cells and deregulated in the paclitaxel-resistant MCF-7Tax(R) cells |
| 25961928 | Crucially, resembling paclitaxel treatment, silencing of FOXM1 and KIF20A similarly promotes abnormal mitotic spindle morphology and chromosome alignment, which have been shown to induce mitotic catastrophe-dependent senescence |
| 25961928 | The physiological relevance of the regulation of KIF20A by FOXM1 is further highlighted by the strong and significant correlations between FOXM1 and KIF20A expression in breast cancer patient samples |
| 25961928 | Statistical analysis reveals that both FOXM1 and KIF20A protein and mRNA expression significantly associates with poor survival, consistent with a role of FOXM1 and KIF20A in paclitaxel action and resistance |
| 25961928 | Collectively, our findings suggest that paclitaxel targets the FOXM1-KIF20A axis to drive abnormal mitotic spindle formation and mitotic catastrophe and that deregulated FOXM1 and KIF20A expression may confer paclitaxel resistance |
| 25686834 | We discovered that miR-34a potently targeted c-Myc and FoxM1, both of which were involved in the activation of telomerase reverse transcriptase (hTERT) transcription, essential for the sustaining activity of telomerase to avoid senescence |
| 25355277 | It was also found that the senescent MSCs (induced by HG glucose) exhibited a marked downregulation in ERK activity and forkhead box M1 (FOXM1) expression, which was reversed by ISDN preconditioning |
| 25355277 | Of note, the inhibition of ERK phosphorylation or the downregulation of FOXM1 statistically abolished the favourable effects of ISDN |
| 25355277 | Furthermore, the downregulation of ERK phosphorylation or FOXM1 expression decreased the miR-130b expression level; however, the suppression of miR-130b demonstrated no significant impact on ERK phosphorylation or FOXM1 expression |
| 25355277 | Taken together, to the best of our knowledge, the present study is the first to demonstrate the favourable effects of ISDN against HG-induced MSC senescence, which are mediated through the activation of the ERK/FOXM1 pathway and the upregulation of miR-130b |
| 25071344 | Down-regulation of FoxM1 inhibits viability and invasion of gallbladder carcinoma cells, partially dependent on inducement of cellular senescence |
| 25071344 | AIM: To investigate the effect of knockdown of Forkhead box M1 (FoxM1) on the proliferation and invasion capacities of human gallbladder carcinoma (GBC)-SD cells |
| 25071344 | METHODS: Four FoxM1 shRNAs were transfected into GBC-SD cells with Lipofectamine 2000 to select the appropriate shRNA for down-regulation of FoxM1 |
| 25071344 | To verify the involvement of FoxM1 in the senescence of tumor cells, staining of senescence beta-galactosidase (SA beta-gal), the widely used biomarker of cellular senescence, was also performed |
| 25071344 | The recombinant adenovirus was then constructed with the shF1822 and successfully transfected into the GBC-SD cells, resulting in the significant inhibition of FoxM1 expression at both the mRNA and protein levels, compared with the negative control (P < 0 |
| 25071344 | After transfection, down-regulation of FoxM1 significantly inhibited cell viability according to the MTT assay (P < 0 |
| 25071344 | SA beta-gal staining showed that down-regulation of FoxM1 could induce more senescent GBC cells (P < 0 |
| 25071344 | CONCLUSION: FoxM1 is functionally involved in viability of GBC cells, partially dependent on the inducement of cellular senescence, and is a potential target for GBC therapy |
| 25068996 | FOXM1: A key oncofoetal transcription factor in health and disease |
| 25068996 | Forkhead Box M1 (FOXM1) is a bona fide oncofoetal transcription factor, which orchestrates complex temporal and spatial gene expression throughout embryonic and foetal development as well as during adult tissue homeostasis and repair |
| 25068996 | Controlled FOXM1 expression and activity provides a balanced transcriptional programme to ensure proper growth and maturation during embryogenesis and foetal development as well as to manage appropriate homeostasis and repair of adult tissues |
| 25068996 | Conversely, deregulated FOXM1 upregulation likely affects cell migration, invasion, angiogenesis, stem cell renewal, DNA damage repair and cellular senescence, which impact tumour initiation, progression, metastasis, angiogenesis and drug resistance |
| 25068996 | A thorough understanding of the regulation and role of FOXM1 in health and in cancer should contribute to the development of better diagnostics and treatments for cancer as well as congenital disorders and other developmental diseases |
| 24981831 | We discuss how B-MYB acts, as the gatekeeper, to coordinate transit through the cell cycle, in conjunction with the multivulval class B (MuvB) complex and FOXM1 transcription factors |
| 24141789 | FOXM1 is implicated in genotoxic drug resistance but its mechanism of action remains elusive |
| 24141789 | Conversely, reconstitution of FOXM1 in FOXM1-deficient MEFs alleviates the accumulation of senescence-associated gammaH2AX foci |
| 24045179 | LEE011 caused cell-cycle arrest and cellular senescence that was attributed to dose-dependent decreases in phosphorylated RB and FOXM1, respectively |
| 23907611 | In contrast, expression of Plk1, an upstream regulator of the cyclin B1/Cdk1 complex, or FoxM1 (forkhead box M1), a master transcriptional factor for the cell cycle regulators of G2/M phase, restored the cell cycle in these cells |
| 23870513 | FOXM1 (Forkhead box M1) in tumorigenesis: overexpression in human cancer, implication in tumorigenesis, oncogenic functions, tumor-suppressive properties, and target of anticancer therapy |
| 23870513 | FOXM1 (Forkhead box M1) is a typical proliferation-associated transcription factor and is also intimately involved in tumorigenesis |
| 23870513 | Additionally, FOXM1 is required for proper execution of mitosis |
| 23870513 | In accordance with its role in stimulation of cell proliferation, FOXM1 exhibits a proliferation-specific expression pattern and its expression is regulated by proliferation and anti-proliferation signals as well as by proto-oncoproteins and tumor suppressors |
| 23870513 | Since these factors are often mutated, overexpressed, or lost in human cancer, the normal control of the foxm1 expression by them provides the basis for deregulated FOXM1 expression in tumors |
| 23870513 | Accordingly, FOXM1 is overexpressed in many types of human cancer |
| 23870513 | FOXM1 is intimately involved in tumorigenesis, because it contributes to oncogenic transformation and participates in tumor initiation, growth, and progression, including positive effects on angiogenesis, migration, invasion, epithelial-mesenchymal transition, metastasis, recruitment of tumor-associated macrophages, tumor-associated lung inflammation, self-renewal capacity of cancer cells, prevention of premature cellular senescence, and chemotherapeutic drug resistance |
| 23870513 | However, in the context of urethane-induced lung tumorigenesis, FOXM1 has an unexpected tumor suppressor role in endothelial cells because it limits pulmonary inflammation and canonical Wnt signaling in epithelial lung cells, thereby restricting carcinogenesis |
| 23870513 | Accordingly, FOXM1 plays a role in homologous recombination repair of DNA double-strand breaks and maintenance of genomic stability, that is, prevention of polyploidy and aneuploidy |
| 23870513 | The implication of FOXM1 in tumorigenesis makes it an attractive target for anticancer therapy, and several antitumor drugs have been reported to decrease FOXM1 expression |
| 23804320 | Activated ERK/FOXM1 pathway by low-power laser irradiation inhibits UVB-induced senescence through down-regulating p21 expression |
| 23804320 | The effect of LPLI was further enhanced with an overexpression of FOXM1, and abolished when FOXM1 was knockdown with short hairpin RNA (shRNA) |
| 23804320 | Furthermore, LPLI activated the extracellular regulated protein kinases (ERK) that was upstream of FOXM1 |
| 23804320 | This led to FOXM1 phosphorylation and nuclear translocation |
| 23804320 | Nuclear translocation enhanced FOXM1 transcriptional activity and promoted its downstream target gene c-Myc expression that could inhibit p21 expression |
| 23804320 | These findings highlight the protective effects of ERK/FOXM1 pathway against UVB-induced cell senescence, suggesting a potential protecting strategy for treating skin aging by LPLI |
| 23262037 | Negative regulation of transcription factor FoxM1 by p53 enhances oxaliplatin-induced senescence in hepatocellular carcinoma |
| 23262037 | Furthermore, inhibition of FoxM1, combined with oxaliplatin treatment, could significantly promote the senescence of HCC cells |
| 19235838 | The FoxM1 transcription factor, a master regulator of mitotic gene expression, promotes the pathogenesis of several malignancies |
| 19235838 | In the present study we determined whether FoxM1 is over-expressed in gastric cancer, and whether it is required to maintain an immortal phenotype of gastric cancer cells |
| 19235838 | The over-expression of FoxM1 was observed in 37/42 tumour specimens from patients with gastric cancer |
| 19235838 | When FoxM1 in gastric cancer cells was knocked-down, impaired clonogenicity and cellular senescence occurred independently of p53 and p16 status |
| 19235838 | FoxM1 depletion led to the down-regulation of its target genes c-MYC and Skp2, coupled with the accumulation of the CDK inhibitor p27(kip1) |
| 19235838 | Taken together, the FoxM1 gene is aberrantly activated in gastric cancer and its inhibition triggers p53- and p16-independent senescence of cancer cells by regulating the expression of p27(kip1) and other targets |
| 19235838 | These findings provide mechanistic insights into the role of FoxM1 in the pathogenesis of gastric cancer, which may have diagnostic and therapeutic implications in gastric cancer |
| 15610763 | Other genes, such as Cdc28 protein kinase 1 (Cks1b), v-myb myeloblastosis viral oncogene homolog (MybL2), pyruvate kinase, muscle 2 (Pkm2) and Forkhead box M1 (FoxM1), were down-regulated only upon TGF-beta1 treatment but not by cellular senescence |
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