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MYBL2 (show MYBL2 Proteins) is a key downstream factor of Akt (show AKT1 Proteins)/FoxM1 signaling to promote progression of human glioma, and could be a new candidate gene for molecular targeting therapy and biomarker for radiotherapy of glioma.
FoxM1 may enhance the invasion and migration of cancer cells, and thus promotes their Epithelialmesenchymal transition, in a mechanism that may involve the regulation of Snai1 (show SNAI1 Proteins).
FoxM1 promotes glioma progression by enhancing UBE2C (show UBE2C Proteins) transcription
We found that, compared with the control, the proliferative, migratory and invasive abilities of PC-3 (show PCSK1 Proteins) cells were decreased after incubation with different concentrations of TMP . The expression of FOXM1 was decreased in TMP-treated PC-3 (show PCSK1 Proteins) cells
FOXM1 expression could be suppressed by miR (show MLXIP Proteins)-216b via direct binding to FOXM1 3'-UTR and miR (show MLXIP Proteins)-216b could inhibit cell proliferation by regulating FOXM1 related Wnt (show WNT2 Proteins)/beta-catenin (show CTNNB1 Proteins) signal pathway. MiR (show MLXIP Proteins)-216b level is related to prognosis in cervical cancer patients and may serve as a potential prognostic marker.
Results revealed that FoxM1 protein was highly expressed in HSCC tissues and that its high expression was closely associated with HSCC tumor differentiation (P=0.004), tumor size (P=0.002), clinical stage (P=0.001), lymph node metastasis (P=0.002), treatment (P=0.045) and expression of the proliferation marker Ki-67 (show MKI67 Proteins) (P<0.001).
Findings suggest that FoxM1 promotes the EMT (show ITK Proteins), invasion and migration of TSCC cells, and cross-talks with c-Met/AKT (show AKT1 Proteins) signaling to form a positive feedback loop to promote TSCC development.
The suppressive activity of miR216b in glioma, which is largely ascribed to downregulation of FoxM1.
our study provide convincing evidences that FoxM1-regulated PBK (show PBK Proteins) exerts oncogenic activities towards HCC (show FAM126A Proteins) via the activation of beta-Catenin (show CTNNB1 Proteins) pathway.
Here we demonstrated that FOXM1 was differentially expressed between MIBC subtypes concordant to its subtype specific expression in breast cancer.
Upregulated ROS (show ROS1 Proteins) induced by FABP4 (show FABP4 Proteins) was of significance in activating FoxM1 leading to airway inflammation and epithelial barrier dysfunction.
Interactions between the Wnt (show WNT2 Proteins)/beta-catenin (show CTNNB1 Proteins) and the Kras/ERK (show EPHB2 Proteins)/Foxm1 pathways are essential to restrict SOX9 (show SOX9 Proteins) expression in basal cells during pulmonary branching morphogenesis
YAP (show YAP1 Proteins) cooperates with FOXM1 to contribute to chromosome instability in hepatocellular carcinoma.
RCM-1 (show TNNI3 Proteins) blocked the nuclear localization and increased the proteasomal degradation of Forkhead box M1 (FOXM1), a transcription factor critical for the differentiation of goblet cells from airway progenitor cells.
These data implicate the insulin (show INS Proteins)-FoxM1/PLK1/CENP-A (show CENPA Proteins) pathway-regulated mitotic cell-cycle progression as an essential component in the beta cell adaptation to delay and/or prevent progression to diabetes.
EGF (show EGF Proteins) promotes FoxM1 expression through the ERK (show EPHB2 Proteins) signal pathway
FoxM1 induction in the pulmonary vasculature was inhibited by a p110gamma (show PIK3CG Proteins)-selective inhibitor and in Pik3cg (show PIK3CG Proteins)(-/-) mice after LPS (show TLR4 Proteins) challenge. Defective vascular repair in Pik3cg (show PIK3CG Proteins)-/- mice results from impaired FoxM1 expression
we suggest that proper regional decidualization and polyploidy development requires FoxM1 signaling downstream of Hoxa10 (show HOXA10 Proteins) and cyclin D3 (show CCND3 Proteins).
FOXM1 and CENPF (show CENPF Proteins) are master regulators of prostate cancer malignancy, and can serve as drug response markers for antineoplastic drugs efficiency.
Both gain-of-function and loss-of-function TP53 (show TP53 Proteins) mutations contribute to overexpression of FoxM1 in high-grade serous ovarian cancer.
the sequence and expression pattern of FoxM1 (fork head box M1) transcription factor in Xenopus laevis embryos are described
Results suggest that FoxM1 functions to link cell division and neuronal differentiation in early Xenopus embryos.
The protein encoded by this gene is a transcriptional activator involved in cell proliferation. The encoded protein is phosphorylated in M phase and regulates the expression of several cell cycle genes, such as cyclin B1 and cyclin D1. Several transcript variants encoding different isoforms have been found for this gene.
Forkhead, drosophila, homolog-like 16
, HNF-3/fork-head homolog 11
, M-phase phosphoprotein 2
, MPM-2 reactive phosphoprotein 2
, forkhead box protein M1
, forkhead-related protein FKHL16
, hepatocyte nuclear factor 3 forkhead homolog 11
, transcription factor Trident
, winged-helix factor from INS-1 cells
, INS-1 winged helix
, forkhead box M1
, forkhead box protein M1-like
, forkhead homolog 16
, winged-helix transcription factor Trident