FOXM1: From cancer initiation to progression and treatment

Koo, Chuay-Yeng; Muir, Kyle; Lam, Eric W.‐F.

doi:10.1016/j.bbagrm.2011.09.004

Cited by 360 publications

(392 citation statements)

References 106 publications

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“…This molecule that has also been described to participate in apoptosis and DNA repair processes is overexpressed in various types of cancers, including HCC (27). In line with these findings, we found increased FOXM1 expression in DEN-induced hepatocellular adenomas of mice.…”

Section: Discussionsupporting

confidence: 80%

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Effects of Wnt‑1 blockade in DEN‑induced hepatocellular adenomas of mice

et al. 2017

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Abstract. Recent evidence has suggested that downregulation of the Wnt/β-catenin signaling pathway may contribute to the development and growth of HCC. Consequently, elements of this pathway have begun to emerge as potential targets for improving outcomes of anti-HCC. Thus, the present study sought to examine the effects of Wnt-1 blockade using the classical diethylnitrosamine (DEN)-induced chemical carcinogenesis mouse model of HCC. The depletion of Wnt-1 using neutralizing antisera was done for ten consecutive days at the age of 9 months and mice were examined for the following 20 days. At that time, DEN-treated mice had multiple variably-sized hepatic cell adenomas. Anti-Wnt-1 was particularly potent in suppressing the expression of critical elements of the Wnt/β-catenin signaling pathway, such as β-catenin and Frizzled-1 receptor, however, not Dickkopf-related protein 1. This effect co-existed with the suppression of Cyclin D1, FOXM1, NF-κΒ and c-Jun commensurate with proliferation and apoptosis blockade in hepatocellular adenomas, and reduced Bcl-2 and c-Met in the serum of mice. Nonetheless, tumor size and multiplicity were found to be unaffected, suggesting that apoptosis may be equally important to proliferation in the context of counteracting DEN induced hepatocellular adenomas of mice.

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Section: Discussionsupporting

confidence: 80%

“…The expression of the proto-oncogene key cell cycle regulator Forkhead box M1 (FOXM1) (27) was in accordance to ki-67 and Cyclin D1 results. Indeed, by IHC the hepatocellular adenomas in DEN-treated mice showed ample FOXM1 expression.…”

Section: Effects Of Wnt-1 Depletion On Selected Tumor Markersmentioning

confidence: 54%

Effects of Wnt‑1 blockade in DEN‑induced hepatocellular adenomas of mice

et al. 2017

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“…Elevated expression of FOXM1 has been detected in a wide range of human tumors and has been implicated in cellular transformation, tumor initiation and progression (7). Accumulating evidence demonstrates that increased expression of FOXM1 is associated with poor prognosis in various types of cancers (8)(9)(10)(11), including MB (12).…”

Section: Introductionmentioning

confidence: 99%

Inhibition of FOXM1 by thiostrepton sensitizes medulloblastoma to the effects of chemotherapy

et al. 2013

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Abstract. Medulloblastoma (MB) is the most common malignant brain tumor in children and is highly invasive and metastatic. Despite recent advances, most MB patients suffer significant therapy-related morbidity, and the survival rate for patients with metastatic MB remains unsatisfactory. Altered expression of FOXM1 has been detected in many types of cancers, and the inhibition of FOXM1 has been studied as a cancer therapy. In the present study, we evaluated the impact of the inhibition of FOXM1 by thiostrepton in Daoy MB cells. Cells were treated with different concentrations of thiostrepton alone or in combination with cisplatin. Cell viability was measured with CCK-8 assays, and cell cycle distribution and apoptosis were assessed by flow cytometric analysis. Changes in protein expression were examined by western blotting. RNAi experiments were performed using siRNA oligonucleotides. The invasion and migration studies were performed using 8-µm Transwell plates. Inhibition of FOXM1 by thiostrepton significantly decreased MB cell proliferation. Cell arrest at the G2/M phase and apoptosis were significantly increased in MB cell lines that were treated with thiostrepton or transfected with siRNA. Thiostrepton decreased the IC 50 value of cisplatin for MB treatment by enhancing cisplatininduced apoptosis. Thiostrepton also decreased cell invasion and migration, which are crucial steps for tumor progression. Our data suggest that targeting FOXM1 with small-molecule inhibitors results in potent antitumor activity and chemosensitizing effects in human medulloblastoma cells.

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“…Furthermore, depletion of FoxM1 has been shown to cause mitotic spindle defects, cell cycle arrest, chromosome misaggregation and mitotic catastrophe [12,13]. Recent reports have also demonstrated that FoxM1 plays important roles in cellular developmental pathways including the maintenance of homeostasis between cell proliferation and apoptosis and as a result, alterations in FoxM1 signaling has been reported to be associated with carcinogenesis and tumor aggressiveness [8,9,14] cancer, glioblastomas, prostate cancer, basal cell carcinomas and pancreas cancer [15][16][17][18][19]. These results give rise to some questions about the role of FoxM1 in pathogenesis of leukemia.…”

Section: Introductionmentioning

confidence: 99%

Targeting FoxM1 transcription factor in T-cell acute lymphoblastic leukemia cell line

et al. 2015

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The Forkhead box protein M1 (FoxM1) is an important transcription factor having significant roles in various cellular events. FoxM1 overexpression has been reported to be related with many types of cancer. However, it is not known whether it contributes to oncogenesis of acute lymphoblastic leukemia. Siomycin A, a thiazol antibiotic, is known to inhibit FoxM1 transcriptional activity. In this study, we aimed to determine gene expression levels of FoxM1 in Jurkat cells (T-cell acute lymphoblastic leukemia cell line) and therapeutic potential of targeting FoxM1 by siomycin A alone and in combination with dexamethasone which improves the survival of children with T-cell acute lymphoblastic leukemia (ALL). We also examined the molecular mechanisms of siomycin A and dexamethasone-induced cell death in Jurkat cells. We demonstrated that FoxM1 mRNA is highly expressed in Jurkat cells. Dexamethasone and siomycin A caused a significant reduction in gene expression levels of FoxM1 in Jurkat cells. Targeting FoxM1 by siomycin A and dexamethasone caused a significant decrease in T-ALL cell line proliferation through induction of G1 cell cycle arrest. All these findings suggest a possible role of FoxM1 in T-cell ALL pathogenesis and represent FoxM1 as an attractive target for T-cell ALL therapy. © 2014 Elsevier Ltd.Dokuz Eylul University Scientific Research Projects Coordination Unit (99.3456.23

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FOXM1: From cancer initiation to progression and treatment

Cited by 360 publications

References 106 publications

Effects of Wnt‑1 blockade in DEN‑induced hepatocellular adenomas of mice

Effects of Wnt‑1 blockade in DEN‑induced hepatocellular adenomas of mice

Inhibition of FOXM1 by thiostrepton sensitizes medulloblastoma to the effects of chemotherapy

Targeting FoxM1 transcription factor in T-cell acute lymphoblastic leukemia cell line

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