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

Wang, Zhiwei; Ahmad, Aamir; Li, Yiwei; Banerjee, Sanjeev; Kong, Dejuan; Sarkar, Fazlul H.

doi:10.1016/j.ctrv.2009.11.006

Cited by 141 publications

(116 citation statements)

References 72 publications

Supporting

Mentioning

114

Contrasting

Order By: Relevance

“…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%

“…The newly developed targeted therapies, if proven effective, may eventually allow us to minimize conventional antineoplastics and the associated toxicities, while maximizing survival and minimizing relapse [5]. The Forkhead box protein M1 (FoxM1) belongs to the Forkhead superfamily of transcription factors which all share an evolutionary conserved 'winged helix' DNA-binding domain [8,9]. The expression of FoxM1 is restricted to cells that are proliferating and its expression is negatively regulated in terminally differentiated cells.…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

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

et al. 2015

View full text Add to dashboard Cite

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

show abstract

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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

et al. 2015

View full text Add to dashboard Cite

show abstract

“…A number of anticancer drugs used in the clinic, function through modulation of cell cycle. In addition to direct targeting of cell cycle regulatory factors for anticancer therapy, genes such as FoxM1 that modulate cell cycle machinery (Wang et al, 2010a), have also been targeted in breast cancer models leading to the inhibition of proliferation and invasion of aggressive cells (Ahmad et al, 2010). Furthermore, the anticancer properties of natural non-toxic compounds are increasingly being realized.…”

Section: Discussionmentioning

confidence: 99%

Cell Cycle Regulatory Proteins in Breast Cancer: Molecular Determinants of Drug Resistance and Targets for Anticancer Therapies

Ahmad¹,

Wang²,

Ali³

et al. 2012

Targeting New Pathways and Cell Death in Breast Cancer

Self Cite

View full text Add to dashboard Cite

“…All Fox members, being classified as FOXA to FOXR (15), Fox molecules play critical roles in a variety of physiologic (16) or pathologic processes such as cancer, as tumor suppressors (17)(18)(19). Particularly, FOXM1 was identified to be oncogenic in pancreatic cancer, and is associated with poor prognosis and pathologic stage of PADC (20,21), whereas, FOXL1 has recently been recognized as a tumor suppressor in PADC (22).…”

Section: Introductionmentioning

confidence: 99%

Co-expression of FOXL1 and PP2A inhibits proliferation inducing apoptosis in pancreatic cancer cells via promoting TRAIL and reducing phosphorylated MYC

Sheng

et al. 2016

Oncology Reports

View full text Add to dashboard Cite

Abstract. Pancreatic cancer is usually diagnosed in the advanced stages and is sensitive to only few therapies. The forkhead box L1 (FOXL1) and protein phosphatase 2A (PP2A) have been recognized to be tumor suppressive in human pancreatic cancers. In the present study, we co-expressed the two tumor suppressive molecules with a '2A peptide' linker, which guaranteed the two molecules were transcribed into one mRNA, whereas they were translated into two separate proteins, in pancreatic cancer Panc-1 cells, and investigated the inhibition of the two molecules on the proliferation and migration of Panc-1 cells. Results demonstrated that, either overexpression of FOXL1 or PP2A via adenovirus significantly inhibited the proliferation of Panc-1 cells, whereas promoted apoptosis in such cells. Moreover, the co-expression of both FOXL1 and PP2A exerted synergistic antitumor effect in Panc-1 cells, with significantly higher proliferation inhibition and tumor induction. In addition, we found that the overexpressed FOXL1 promoted the TNF-related apoptosis-inducing ligand (TRAIL), whereas the overexpressed PP2A downregulated the phosphorylation of c-MYC. The co-expression of FOXL1 and PP2A presented both functions in Panc-1 cells. In conclusion, the adenovirus-mediated co-expression of FOXL1 and PP2A with the 2A peptide linker exterts synergistic suppression of pancreatic cancer cells via inhibiting the growth and promoting apoptosis of cancer cells, probably via upregulating TRAIL and reducing the phosphorylation of MYC.

show abstract

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

Cited by 141 publications

References 72 publications

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

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

Cell Cycle Regulatory Proteins in Breast Cancer: Molecular Determinants of Drug Resistance and Targets for Anticancer Therapies

Co-expression of FOXL1 and PP2A inhibits proliferation inducing apoptosis in pancreatic cancer cells via promoting TRAIL and reducing phosphorylated MYC

Contact Info

Product

Resources

About