FoxM1: A Master Regulator of Tumor Metastasis

Raychaudhuri, Pradip; Park, Hyun Jung

doi:10.1158/0008-5472.can-11-0640

Cited by 276 publications

(254 citation statements)

References 30 publications

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“…S4). FOXM1 is frequently associated with metastasis and patient survival in many types of cancers (28,29); it was also reported that FOXM1 activity was significantly increased in bladder cancers relative to normal bladder tissues and might have a prognostic value at the individual level (30). CCNB1, a downstream effector of FOXM1, is upregulated and is known to be a prognostic biomarker in many cancers (25)(26)(27).…”

Section: Discussionmentioning

confidence: 98%

Expression Signature Defined byFOXM1–CCNB1Activation Predicts Disease Recurrence in Non–Muscle-Invasive Bladder Cancer

Kim

Roh

Park

et al. 2014

Clinical Cancer Research

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Purpose: Although standard treatment with transurethral resection and intravesical therapy (IVT) is known to be effective to address the clinical behavior of non–muscle-invasive bladder cancer (NMIBC), many patients fail to respond to the treatment and frequently experience disease recurrence. Here, we aim to identify a prognostic molecular signature that predicts the NMIBC heterogeneity and response to IVT. Experimental Design: We analyzed the genomic profiles of 102 patients with NMIBC to identify a signature associated with disease recurrence. The validity of the signature was verified in three independent patient cohorts (n = 658). Various statistical methods, including a leave-one-out cross-validation and multivariate Cox regression analyses, were applied to identify a signature. We confirmed an association between the signature and tumor aggressiveness with experimental assays using bladder cancer cell lines. Results: Gene expression profiling in 102 patients with NMIBC identified a CCNB1 signature associated with disease recurrence, which was validated in another three independent cohorts of 658 patients. The CCNB1 signature was shown to be an independent risk factor by a multivariate analysis and subset stratification according to stage and grade [HR, 2.93; 95% confidence intervals (CI), 1.302–6.594; P = 0.009]. The subset analysis also revealed that the signature could identify patients who would benefit from IVT. Finally, gene network analyses and experimental assays indicated that NMIBC recurrence could be mediated by FOXM1–CCNB1–Fanconi anemia pathways. Conclusions: The CCNB1 signature represents a promising diagnostic tool to identify patients with NMIBC who have a high risk of recurrence and to predict response to IVT. Clin Cancer Res; 20(12); 3233–43. ©2014 AACR.

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Section: Discussionmentioning

confidence: 98%

Expression Signature Defined byFOXM1–CCNB1Activation Predicts Disease Recurrence in Non–Muscle-Invasive Bladder Cancer

Kim

Roh

Park

et al. 2014

Clinical Cancer Research

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“…Accumulating evidence shows that activation of FOXM1 is associated with the development of human cancers (33)(34)(35). FOXM1 is a FOX transcription factor that regulates a number of cell cycle regulators (33,34,36,37).…”

Section: Discussionmentioning

confidence: 99%

“…FOXM1 is a FOX transcription factor that regulates a number of cell cycle regulators (33,34,36,37). Several studies have shown that FOXM1 is overexpressed in tumors including lung, liver and breast cancers and is associated with prognosis (38)(39)(40).…”

Section: Discussionmentioning

confidence: 99%

3,3′-Diindolylmethane potentiates paclitaxel-induced antitumor effects on gastric cancer cells through the Akt/FOXM1 signaling cascade

2015

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Abstract. Gastric cancer is the fourth most common cancer and is one of the leading causes of cancer-related mortality worldwide. Forkhead box M1 (FOXM1) is overexpressed in gastric cancer, suggesting that it is important in gastric cancer oncogenesis. However, no studies have investigated the role of 3,3'-diindolylmethane (DIM), a component of cruciferous vegetables, in the regulation of FOXM1 and its signaling pathway in gastric cancer. Here, we report for the first time that DIM effectively downregulated Akt/FOXM1 in gastric cancer cells. Combination treatment with DIM and paclitaxel significantly and dose-dependently inhibited the proliferation of SNU638 cells when compared to treatment with DIM or paclitaxel alone. Colony formation of SNU638 cells was significantly attenuated by treatment with DIM and paclitaxel, and DIM potentiated the inhibition of colony formation in SNU638 cells by paclitaxel when compared to treatment with a single agent. Treatment with DIM plus paclitaxel substantially increased apoptosis as indicated by increased levels of cleaved polyADP-ribose polymerase (PARP) and cleaved caspase-9 protein. DIM dose-dependently sensitized gastric cancer cells through downregulation of FOXM1 and potentiated the effects of paclitaxel. FOXM1 effector genes such as CDK4, p53 and cyclin D1 were downregulated in gastric cancer cells by combination treatment with DIM and paclitaxel. In addition, DIM significantly and dose-dependently inhibited phosphorylation of Akt and potentiated paclitaxel-induced inhibition of Akt function in gastric cancer cells. Therefore, our results indicate that DIM effectively potentiates the efficacy of chemotherapeutic agents such as paclitaxel by downregulation of the Akt/ FOXM1 signaling cascade in gastric cancer cells. Our findings suggest that DIM enhances the therapeutic efficacy of paclitaxel in gastric cancer and is a potential clinical anticancer agent for the prevention and/or treatment of gastric cancer.

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“…Reactive oxygen species (ROS) trigger expression of FoxM1 and interestingly, FoxM1 also triggers expression of ROS scavengers such as Superoxide Dismutase (SOD), Catalase [6,7]. Overexpression of FoxM1 renders cancer cells resistance to ROSmediated cell death.…”

Section: Introductionmentioning

confidence: 99%

Hardaliyenin HT-29, DU-145, HeLa Kanser Hücreleri ve CF-1 (Fare Embriyonik Fibroblast) Hücresi FoxM1 Gen Expresyon Seviyelerine Etkisi

Kahraman-Ilıkkan¹

2017

Akademik Gıda

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Chemotherapeutic agents may influence both cancer cells and healthy cells, therefore alternative therapeutic agents or targets have become a milestone of cancer cure. Forkhead box M1 (FoxM1) is a transcriptional regulator and a novel cancer therapy target as overexpressed in cancer cells, and its inhibitors are considered as potential therapeutic agents to halt cancer progression. Therefore, in this study, the effect of "Hardaliye" on cancer cells and a healthy cell line was primarily investigated by MTT (3(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium-bromide) and later on, FoxM1 gene expression levels were determined. Hardaliye, especially when diluted ten and twenty-fold, decreased viability percentage of all cancer cells and did not affect healthy cells. FoxM1 levels of cancer cells drastically decreased especially in HT-29 cells while did not statistically change their levels in the healthy cell line.

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FoxM1: A Master Regulator of Tumor Metastasis

Cited by 276 publications

References 30 publications

Expression Signature Defined byFOXM1–CCNB1Activation Predicts Disease Recurrence in Non–Muscle-Invasive Bladder Cancer

Expression Signature Defined byFOXM1–CCNB1Activation Predicts Disease Recurrence in Non–Muscle-Invasive Bladder Cancer

3,3′-Diindolylmethane potentiates paclitaxel-induced antitumor effects on gastric cancer cells through the Akt/FOXM1 signaling cascade

Hardaliyenin HT-29, DU-145, HeLa Kanser Hücreleri ve CF-1 (Fare Embriyonik Fibroblast) Hücresi FoxM1 Gen Expresyon Seviyelerine Etkisi

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