Interplay between the NF-κB and forkhead transcription factors

Peng, Stanford L.

doi:10.1038/sj.cdd.4401640

Cited by 6 publications

(5 citation statements)

References 10 publications

(5 reference statements)

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“…Because some Fox transcription factors reportedly modulate NF-κB in non-malignant conditions (27), we postulated that FOXC1 might modulate NF-κB function in BLBC cells. Using immunoblotting, we found that the NF-κB p65 subunit and its phosphorylation at Ser-546 (by IκB kinase [IKK]) were markedly induced by FOXC1 overexpression in basal-like MDA-MB-231 breast cancer cells (Figure 1B) and luminal MCF-7 breast cancer cells (Supplemental Figure 1A), which harbor low and undetectable endogenous FOXC1 levels, respectively (12).…”

Section: Resultsmentioning

confidence: 99%

FOXC1 regulates the functions of human basal-like breast cancer cells by activating NF-κB signaling

et al. 2012

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Human basal-like breast cancer (BLBC) is an enigmatic and aggressive malignancy with a poor prognosis. There is an urgent need to identify therapeutic targets for BLBC because current treatment modalities are limited and not effective. The forkhead box transcription factor FOXC1 has recently been identified as a critical functional biomarker for BLBC. However, how it orchestrates BLBC cells was not clear. Here we show that FOXC1 activates the transcription factor NF-κB in BLBC cells by increasing p65/RelA protein stability. High NF-κB activity has been associated with estrogen receptor-negative breast cancer, particularly BLBC. The effect of FOXC1 on p65/RelA protein stability is mediated by increased expression of Pin1, a peptidyl-prolyl isomerase. FOXC1 requires NF-κB for its regulation of cell proliferation, migration, and invasion. Notably, FOXC1 overexpression renders breast cancer cells more susceptible to pharmacologic inhibition of NF-κB. These results suggest that BLBC cells may rely on FOXC1-driven NF-κB signaling. Interventions of this pathway may provide modalities for the treatment of BLBC.

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Section: Resultsmentioning

confidence: 99%

FOXC1 regulates the functions of human basal-like breast cancer cells by activating NF-κB signaling

et al. 2012

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“…FoxM1 has been shown to activate the oncogenic pathways that are important in carcinogenesis such as mitogen activated protein kinase (MAPK), extracellular signal-regulated kinase (ERK), phosphatdyl inositol 3-kinase (PI3k)/Akt), nuclear factor kappa-B and sonic hedgehog (SHH) [33][34][35][36][37]. Moreover, FoxM1 has been shown to decrease the gene expression levels of the tumor suppressor genes and also the genes involved in cellular senescence like p53 and p21 cip1 [20,38].…”

Section: Discussionmentioning

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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“…It has been reported that the interplay between the NF-κB and forkhead transcription factors, such as Foxj1, Foxo3a and Foxp3 is biologically important. For example, Foxo3a promotes cell apoptosis through regulation of IκBβ and suppression of NF-κB 26. Recently, Penzo et al reported that inhibition of NF-κB by IκBα super repressor in the MEFs abrogated both the IKKβ mediated induction of direct NF-κB targets and the repression effect on the FoxM1 targets 27.…”

Section: Foxm1 and Nf-κb Signalingmentioning

confidence: 99%

Forkhead box M1 transcription factor: A novel target for cancer therapy

Wang

Ahmad

et al. 2010

Cancer Treatment Reviews

141

114

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FoxM1 signaling has been reported to be associated with carcinogenesis. Therefore, the FoxM1 may represent a novel therapeutic target, and thus the development of agents that will target FoxM1 is likely to have significant therapeutic impact on human cancer. This review describes the mechanisms of signal transduction associated with FoxM1 and provides emerging evidence in support of its role in the carcinogenesis. Further, we summarize data on several FoxM1 inhibitors especially “chemopreventive agents” and these agents could be useful for targeted inactivation of FoxM1, which indeed could become a novel approach for the prevention and/or treatment of human cancer.

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Interplay between the NF-κB and forkhead transcription factors

Cited by 6 publications

References 10 publications

FOXC1 regulates the functions of human basal-like breast cancer cells by activating NF-κB signaling

FOXC1 regulates the functions of human basal-like breast cancer cells by activating NF-κB signaling

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

Forkhead box M1 transcription factor: A novel target for cancer therapy

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