Homo sapiens forkhead box M1 (FOXM1), novel transcript variant FOXM1D, complete cds
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ABSTRACT:
PROVIDER: PRJEB24591 | ENA |
REPOSITORIES: ENA
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Project description:Forkhead Box M1 (FOXM1) is a promising molecular target for high-risk multiple myeloma and relapse and refractory myeloma, but whether FOXM1 is essential in myeloma has not yet been established. To address this knowledge gap, we used Western blotting to measure FOXM1 protein levels in 11 human myeloma cell lines (HMCLs) and then chose the two lines expressing the largest amount of the transcription factor, OPM2 and Delta47, for gene editing using CRISPR-Cas9. In both cases, two independent FOXM1-deficient daughter lines, designated KO-1 and KO-2, were generated. They contained 2 different 10-bp deletions at the target site of their respective guide RNA in case of OPM2 and a 10-bp deletion and 1-bp insertion in case of Delta47. Western analysis confirmed the lack of FOXM1 in all knockout clones. FOXM1-deficient myeloma cells proliferated more slowly than their parental counterparts containing normal levels of FOXM1. Moreover, we added back FOXM1 to FOXM1-KO cells by transfection of a constitutively expressed FOXM1c cDNA gene. The reconstituted OPM2 and Delta47 cells, designated FOXM1 KO-R contained high amounts of FOXM1 protein. Here, we used these cell lines to investigate the role of FOXM1 in regulating the gene expression in multiple myeloma.
2021-07-14 | GSE180018 | GEO
Project description:Effect of forkhead box M1 in multiple myeloma
| PRJNA746277 | ENA
Project description:Human embryonic stem cells (hESCs) exhibit unique cell cycle structure, self-renewal and pluripotency. The Forkhead box transcription factor M1 (FOXM1) is critically required for the maintenance of pluripotency in mouse embryonic stem cells and mouse embryonal carcinoma cells, but its role in hESCs remains unclear. Here, we show that FOXM1 expression was enriched in undifferentiated hESCs and was regulated in a cell cycle-dependent manner with peak levels detected at the G2/M phase. Expression of FOXM1 did not correlate with OCT4 and NANOG during in vitro differentiation of hESCs. Importantly, knockdown of FOXM1 expression led to aberrant cell cycle distribution with impairment in mitotic progression but showed no profound effect on the undifferentiated state. Interestingly, FOXM1 depletion sensitized hESCs to oxidative stress. Moreover, genome-wide analysis of FOXM1 targets by ChIP-seq identified genes important for M phase including CCNB1 and CDK1, which were subsequently confirmed by ChIP and RNA interference analyses. Further peak set comparison against a differentiating hESC line and a cancer cell line revealed substantial difference in the genomic binding profile of FOXM1 in hESCs. Taken together, our findings provide the first evidence to support FOXM1 as important regulator of cell cycle progression and defense against oxidative stress in hESCs.
2016-04-08 | GSE79694 | GEO
Project description:Rosmarinic acid methyl ester (RAME), a derivative of rosmarinic acid (RA), has been reported to have several therapeutic effects, including anti-tumor effects, against cervical cancer. However, its anti-tumor effects in ovarian cancer is unclear. In this study, we studied the molecular pathways associated with the anti-tumor effects of RAME in ovarian cancer. To identify the effects of RAME in ovarian cancer, RNA sequencing was performed in RAME-treated ovarian cancer cells; we found that RAME treatment downregulated genes closely involved with the target genes of the transcription factor Forkhead box M1 (FOXM1). It has been reported that FOXM1 is overexpressed in a variety of cancer cells and is associated with cell proliferation and tumorigenesis. Therefore, we hypothesized that FOXM1 is a key target of RAME; this can result in its anti-tumor effects. Treatment of ovarian cancer cells with RAME inhibited cell migration and invasion, as shown by wound healing and transwell migration assays. To examine whether RAME represses the action of FOXM1, we performed quantitative RT-PCR and ChIP-qPCR. Treatment of ovarian cancer cells with RAME decreased the mRNA expression of FOXM1 target genes and the binding of FOXM1 to its target genes. Moreover, FOXM1 expression was increased in cisplatin-resistant ovarian cancer cells, and combination treatment with RAME and cisplatin sensitized the cisplatin-resistant ovarian cancer cells, which was likely due to FOXM1 inhibition. Our research suggests that RAME is a promising option in treating ovarian cancer patients by revealing a novel molecular pathway underlying its anti-tumor effects.
2020-09-28 | GSE158604 | GEO
Project description:Rattus norvegicus Foxm1, forkhead box M1 [Source:RGD Symbol;Acc:61807], is differentially expressed in 13 experiment(s);
| ENSRNOG00000005936 | ExpressionAtlas
Project description:Rattus norvegicus Foxm1, forkhead box M1 [Source:RGD Symbol;Acc:61807], is expressed in 2 baseline experiment(s);
| ENSRNOG00000005936 | ExpressionAtlas
Project description:Sus scrofa FOXM1, forkhead box M1 [Source:VGNC Symbol;Acc:VGNC:88217], is differentially expressed in 1 experiment(s);
| ENSSSCG00000000739 | ExpressionAtlas
Project description:Sus scrofa FOXM1, forkhead box M1 [Source:VGNC Symbol;Acc:VGNC:88217], is expressed in 2 baseline experiment(s);
| ENSSSCG00000000739 | ExpressionAtlas
Project description:Macaca mulatta FOXM1, forkhead box M1 [Source:VGNC Symbol;Acc:VGNC:72702], is expressed in 2 baseline experiment(s);
| ENSMMUG00000019385 | ExpressionAtlas
Project description:Homo sapiens FOXM1, forkhead box M1 [Source:HGNC Symbol;Acc:HGNC:3818], is differentially expressed in 241 experiment(s);
| ENSG00000111206 | ExpressionAtlas