scholarly journals Prognostic Significance of Forkhead Box M1 (FOXM1) Expression and Antitumor Effect of FOXM1 Inhibition in Angiosarcoma

2016 ◽  
Vol 7 (7) ◽  
pp. 823-830 ◽  
Author(s):  
Takamichi Ito ◽  
Kenichi Kohashi ◽  
Yuichi Yamada ◽  
Takeshi Iwasaki ◽  
Akira Maekawa ◽  
...  
Keyword(s):  
Antitumor Effect ◽  
Prognostic Significance ◽  
Forkhead Box ◽  
Forkhead Box M1 ◽  
Foxm1 Expression

scholarly journals Prognostic significance of forkhead box M1 (FoxM1) expression and antitumour effect of FoxM1 inhibition in melanoma

2016 ◽  
Vol 69 (1) ◽  
pp. 63-71 ◽  
Author(s):  
Takamichi Ito ◽  
Kenichi Kohashi ◽  
Yuichi Yamada ◽  
Akira Maekawa ◽  
Masaaki Kuda ◽  
...  
Keyword(s):  
Prognostic Significance ◽  
Antitumour Effect ◽  
Forkhead Box ◽  
Forkhead Box M1 ◽  
Foxm1 Expression

Suppression of human HCC cell growth in vitro by siRNA silencing of forkhead box M1 expression.

2013 ◽  
Vol 31 (4_suppl) ◽  
pp. 173-173
Author(s):  
Keon Uk Park ◽  
Ji Hong Kim ◽  
Hye-Jin Kim ◽  
Yun-Han Lee
Keyword(s):  
Cell Growth ◽  
Hepg2 Cells ◽  
Cell Cycle Progression ◽  
Apoptotic Cell ◽  
Mrna Level ◽  
Forkhead Box ◽  
Forkhead Box M1 ◽  
Expression Of Genes ◽  
Foxm1 Expression

173 Background: Development of targeted therapy for hepatocellular carcinoma (HCC) remains a major challenge. The transcription factor forkhead box M1 (FOXM1) is a member of the forkhead family, and it induces the expression of genes involved in the execution of mitosis. Liver regeneration studies that used the albumin promoter/enhancer cre recombinase (Alb-Cre) transgene to mediate hepatocyte-specific deletion of the mouse Foxm1 LoxP/LoxP targeted allele (Foxm1fl/fl) demonstrated that Foxm1 is required for hepatocyte DNA replication and mitosis. Methods: We explored the possibility of FoxM1 being a potential therapeutic target for HCC.To inactivate target gene expression, Huh7 and HepG2 cells were treated with the various doses of three different siRNAs (FoxM1-1, FoxM1-2 and FoxM1-3). The change of FoxM1 expression in mRNA level was then determined by quantitative real-time PCR. Cell growth was analyzed by MTT assay, and apoptosis was estimated by ELISA for the detection of denatured ssDNA only formed during apoptotic progression. Results: Among the three tested siRNA molecules, the FoxM1-1siRNA was the most effective in inhibiting HCC cell growth. Both Huh7 and HepG2 cells transfected with 15nM of FoxM1-1siRNA showed more than 60% growth inhibition by 4 days. Inhibition of cell growth was due to increased rate of apoptotic cell death which was about 2-fold higher than in untreated control cells. Upregulation of apoptosis directly correlated with down-regulation of FoxM1 mRNA level. Furthermore, siRNA-mediated silencing of FoxM1 expression in HCC cells retarded cell cycle progression. Conclusions: These results indicate that FoxM1 plays a pivotal role in HCC pathogenesis and maybe an attractive molecular target for systemic HCC therapy.

scholarly journals FOXM1: A Multifunctional Oncoprotein and Emerging Therapeutic Target in Ovarian Cancer

Cancers ◽  
2021 ◽  
Vol 13 (12) ◽  
pp. 3065
Author(s):  
Cassie Liu ◽  
Carter J. Barger ◽  
Adam R. Karpf
Keyword(s):  
Ovarian Cancer ◽  
Therapeutic Target ◽  
Current Knowledge ◽  
Chemotherapy Resistance ◽  
Invasion And Metastasis ◽  
Transcriptional Signature ◽  
Forkhead Box ◽  
Forkhead Box M1 ◽  
Foxm1 Expression ◽  
Translational Mechanisms

Forkhead box M1 (FOXM1) is a member of the conserved forkhead box (FOX) transcription factor family. Over the last two decades, FOXM1 has emerged as a multifunctional oncoprotein and a robust biomarker of poor prognosis in many human malignancies. In this review article, we address the current knowledge regarding the mechanisms of regulation and oncogenic functions of FOXM1, particularly in the context of ovarian cancer. FOXM1 and its associated oncogenic transcriptional signature are enriched in >85% of ovarian cancer cases and FOXM1 expression and activity can be enhanced by a plethora of genomic, transcriptional, post-transcriptional, and post-translational mechanisms. As a master transcriptional regulator, FOXM1 promotes critical oncogenic phenotypes in ovarian cancer, including: (1) cell proliferation, (2) invasion and metastasis, (3) chemotherapy resistance, (4) cancer stem cell (CSC) properties, (5) genomic instability, and (6) altered cellular metabolism. We additionally discuss the evidence for FOXM1 as a cancer biomarker, describe the rationale for FOXM1 as a cancer therapeutic target, and provide an overview of therapeutic strategies used to target FOXM1 for cancer treatment.

scholarly journals Differential expression of forkhead box M1 in human epithelial ovarian cancer.

2021 ◽  
Author(s):  
Shahan Mamoor
Keyword(s):  
Ovarian Cancer ◽  
Epithelial Ovarian Cancer ◽  
Fallopian Tube ◽  
Expression Profiles ◽  
High Grade ◽  
Primary Tumors ◽  
Forkhead Box ◽  
Ovarian Cancers ◽  
Forkhead Box M1 ◽  
Foxm1 Expression

Epithelial ovarian cancer (EOC) is the most lethal gynecologic cancer (1). We performed discovery of genes associated with epithelial ovarian cancer and of the high-grade serous ovarian cancer (HGSC) subtype, using published microarray data (2, 3) to compare global gene expression profiles of normal ovary or fallopian tube with that of primary tumors from women diagnosed with epithelial ovarian cancer or HGSC. We identified the gene encoding forkhead box M1, FOXM1, as among the genes whose expression was most different in epithelial ovarian cancer as compared to the normal fallopian tube. FOXM1 expression was significantly higher in high-grade serous ovarian tumors relative to normal fallopian tube. FOXM1 expression correlated with progression-free survival in patients with ovarian cancer. These data indicate that expression of FOXM1 is perturbed in epithelial ovarian cancers broadly and in ovarian cancers of the HGSC subtype. FOXM1 may be relevant to pathways underlying ovarian cancer initiation (transformation) or progression.

scholarly journals Prognostic Value of FOXM1 in Patients with Malignant Solid Tumor: A Meta-Analysis and System Review

2015 ◽  
Vol 2015 ◽  
pp. 1-10 ◽  
Author(s):  
Jun Dai ◽  
Lili Yang ◽  
Jinyu Wang ◽  
Ying Xiao ◽  
Qiurong Ruan
Keyword(s):  
Meta Analysis ◽  
Ductal Adenocarcinoma ◽  
Time To Event ◽  
Small Cell Lung ◽  
Forkhead Box ◽  
Forkhead Box M1 ◽  
Pubmed Database ◽  
Foxm1 Expression ◽  
Malignant Solid Tumor ◽  
System Review

Forkhead box M1 (FOXM1), a member of the Fox transcription factors family, was closely related with cell cycle. FOXM1 played an important role in MST and prompted a poor prognosis for MST patients. However, there were also some studies revealing no significant association between the FOXM1 expression and prognosis of patients. Therefore, we conducted meta-analysis to investigate whether the expression of FOXM1 was associated with MST prognosis. We collected 36 relevant studies through PubMed database and obtained research data of 4946 patients. Stata 12.0 was used to express the results as hazard ratio (HR) for time-to-event outcomes with 95% confidence intervals (95% CI). It was shown that overexpression of FOXM1 was relevant to worse survival of MST patients (HR = 1.99, 95% CI = 1.79–2.21,P<0.001;I2=26.4%,Ph=0.076). Subgroup analysis suggested that overexpression of FOXM1 in breast cancer (BC), gastric cancer (GC), hepatocellular carcinoma (HCC), pancreatic ductal adenocarcinoma (PDA), and non-small-cell lung cancer (NSCLC) all predicted a worse survival (P<0.05), in addition to ovarian cancer (OC) (P=0.084). In conclusion, our research indicated that overexpression of FOXM1 was to the disadvantage of the prognosis for majority of MST and therefore can be used as an evaluation index of prognosis.

scholarly journals Prognostic significance of FOXM1 expression and antitumor effect of FOXM1 inhibition in synovial sarcomas

BMC Cancer ◽  
2016 ◽  
Vol 16 (1) ◽  
Author(s):  
Akira Maekawa ◽  
Kenichi Kohashi ◽  
Masaaki Kuda ◽  
Kunio Iura ◽  
Takeaki Ishii ◽  
...  
Keyword(s):  
Antitumor Effect ◽  
Prognostic Significance ◽  
Foxm1 Expression ◽  
Synovial Sarcomas
Sign in / Sign up

Export Citation Format

Share Document