scholarly journals Knockdown of MALAT1 expression inhibits HUVEC proliferation by upregulation of miR-320a and downregulation of FOXM1 expression

Oncotarget ◽  
2017 ◽  
Vol 8 (37) ◽  
pp. 61499-61509 ◽  
Author(s):  
Jian-Yong Sun ◽  
Zheng-Wei Zhao ◽  
Wei-Miao Li ◽  
Guang Yang ◽  
Peng-Yu Jing ◽  
...  
Keyword(s):  
Foxm1 Expression ◽  
Huvec Proliferation

Aberrant FoxM1 Expression Increases ASPM Transcription and Promotes the Malignant Properties of Gliomas

2019 ◽  
Author(s):  
Wen-Jing Zeng ◽  
Quan Cheng ◽  
Zhi-Peng Wen ◽  
Jie-Ya Wang ◽  
Yan-Hong Chen ◽  
...  
Keyword(s):  
Foxm1 Expression

scholarly journals The Dickkopf1 and FOXM1 positive feedback loop promotes tumor growth in pancreatic and esophageal cancers

Oncogene ◽  
2021 ◽  
Author(s):  
Hirokazu Kimura ◽  
Ryota Sada ◽  
Naoki Takada ◽  
Akikazu Harada ◽  
Yuichiro Doki ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Wnt Signaling ◽  
Cancer Cell ◽  
Positive Feedback ◽  
Feedback Loop ◽  
Ductal Adenocarcinoma ◽  
Cancer Cell Proliferation ◽  
Positive Feedback Loop ◽  
Dkk1 Expression ◽  
Foxm1 Expression

AbstractDickkopf1 (DKK1) is overexpressed in various cancers and promotes cancer cell proliferation by binding to cytoskeleton-associated protein 4 (CKAP4). However, the mechanisms underlying DKK1 expression are poorly understood. RNA sequence analysis revealed that expression of the transcription factor forkhead box M1 (FOXM1) and its target genes concordantly fluctuated with expression of DKK1 in pancreatic ductal adenocarcinoma (PDAC) cells. DKK1 knockdown decreased FOXM1 expression and vice versa in PDAC and esophageal squamous cell carcinoma (ESCC) cells. Inhibition of either the DKK1-CKAP4-AKT pathway or the ERK pathway suppressed FOXM1 expression, and simultaneous inhibition of both pathways showed synergistic effects. A FOXM1 binding site was identified in the 5ʹ-untranslated region of the DKK1 gene, and its depletion decreased DKK1 expression and cancer cell proliferation. Clinicopathological and database analysis revealed that PDAC and ESCC patients who simultaneously express DKK1 and FOXM1 have a poorer prognosis. Multivariate analysis demonstrated that expression of both DKK1 and FOXM1 is the independent prognostic factor in ESCC patients. Although it has been reported that FOXM1 enhances Wnt signaling, FOXM1 induced DKK1 expression independently of Wnt signaling in PDAC and ESCC cells. These results suggest that DKK1 and FOXM1 create a positive feedback loop to promote cancer cell proliferation.

scholarly journals ERβ1 Represses FOXM1 Expression through Targeting ERα to Control Cell Proliferation in Breast Cancer

2011 ◽  
Vol 179 (3) ◽  
pp. 1148-1156 ◽  
Author(s):  
Yoshiya Horimoto ◽  
Johan Hartman ◽  
Julie Millour ◽  
Steven Pollock ◽  
Yolanda Olmos ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cell Proliferation ◽  
Control Cell ◽  
Foxm1 Expression

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 Propofol Inhibits Lung Cancer A549 Cell Growth and Epithelial‐Mesenchymal Transition Process by Upregulation of MicroRNA-1284

2018 ◽  
Vol 27 (1) ◽  
pp. 1-8 ◽  
Author(s):  
Wei-Zhen Liu ◽  
Nian Liu
Keyword(s):  
Lung Cancer ◽  
Cell Viability ◽  
Cancer Cells ◽  
A549 Cell ◽  
Epithelial Mesenchymal Transition ◽  
A549 Cells ◽  
Lung Cancer Cells ◽  
Migration And Invasion ◽  
Mesenchymal Transition ◽  
Foxm1 Expression

Propofol has been widely used in lung cancer resections. Some studies have demonstrated that the effects of propofol might be mediated by microRNAs (miRNAs). This study aimed to investigate the effects and mechanisms of propofol on lung cancer cells by regulation of miR-1284. A549 cells were treated with different concentrations of propofol, while transfected with miR-1284 inhibitor, si-FOXM1, and their negative controls. Cell viability, migration, and invasion, and the expression of miR-1284, FOXM1, and epithelial‐mesenchymal transition (EMT) factors were detected by CCK-8, Transwell, qRT-PCR, and Western blot assays, respectively. In addition, the regulatory and binding relationships among propofol, miR-1284, and FOXM1 were assessed, respectively. Results showed that propofol suppressed A549 cell viability, migration, and invasion, upregulated E-cadherin, and downregulated N-cadherin, vimentin, and Snail expressions. Moreover, propofol significantly promoted the expression of miR-1284. miR-1284 suppression abolished propofol-induced decreases of cell viability, migration, and invasion, and increased FOXM1 expression and the luciferase activity of FOXM1-wt. Further, miR-1284 negatively regulated FOXM1 expression. FOXM1 knockdown reduced cell viability, migration, and invasion by propofol treatment plus miR-1284 suppression. In conclusion, our study indicated that propofol could inhibit cell viability, migration, invasion, and the EMT process in lung cancer cells by regulation of miR-1284.

scholarly journals LncRNA MALAT1 acts as a miR-125a-3p sponge to regulate FOXM1 expression and promote hepatocellular carcinoma progression

2019 ◽  
Vol 10 (26) ◽  
pp. 6649-6659 ◽  
Author(s):  
Shihai Liu ◽  
Jing Qiu ◽  
Guifang He ◽  
Ye Liang ◽  
Liping Wang ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Lncrna Malat1 ◽  
Foxm1 Expression
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