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The tumour suppressive roles of miR8765p overexpression in GBM cells were significantly reversed by FOXM1 reintroduction.
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Data show that forkhead box protein M1 (FoxM1) enhanced carboplatin resistance in Y-79CR cells through directly up-regulating the transcription of ATP-binding cassette transporter C4 (ABCC4).
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FoxM1 repression during human aging leads to mitotic decline and aneuploidy-driven full senescence.
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TBX2 is a neuroblastoma core regulatory circuitry component enhancing MYCN/FOXM1 reactivation of DREAM targets.
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Studies indicate that the oncogene forkhead box protein M1 (FoxM1) has emerged as an important molecule implicated in initiation, development and progression of cancer [Review].
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These findings revealed the role of forkhead box M1 upregulation by manganese superoxide dismutase overexpression in maintaining lung cancer stem-like cell properties. Therefore, inhibition of forkhead box M1 upregulation by manganese superoxide dismutase overexpression may represent an effective therapeutic strategy for non-small cell lung cancer.
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FoxM1 silenced cell induces G2/M cell cycle arrest and necrosis.
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High FOXM1 expression is associated with invasion of renal cancer.
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Analyses with phospho-defective and phospho-mimetic mutants of FoxM1b identified a critical role of the Plk1 phosphorylation sites in regulating the binding of FoxM1b to Rb and DNMT3b.
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Study found that DLX1 was the direct target of FoxM1 in HCC. Downregulation of FoxM1 inhibits the proliferation, migration, and invasion of HCC cells by miR-214.
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A significant over expression of forkhead box protein M1 (FOXM1), polo-like kinase 1 (PLK1) and centrosomal protein 55 (CEP55) was observed in tumor samples compared to adjacent and normal bladder tissues, suggesting they may be potential candidate's biomarkers for early diagnosis and targets for cancer therapy.
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In conclusion, our findings indicated that FOXM1 was highly expressed in lung cancer cells after exposure to ionizing radiation (IR). We also found that FOXM1 promoted radioresistance, invasion, migration, and EMT of lung cancer cells after IR, partly through upregulating KIF20A.
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The concurrent overexpression of FoxM1 and FoxP3 was evident in gastric cancer and inversely correlated with patient survival.
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A better understanding of the mechanisms regulating the FOXO3-FOXM1 axis, as well as their downstream transcriptional targets and functions, may render these proteins reliable and early diagnostic/prognostic factors as well as crucial therapeutic targets for cancer treatment and importantly, for overcoming chemotherapeutic drug resistance.
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CRNDE overexpression accelerated lipopolysaccharide-induced apoptosis and inflammation via up-regulation of FOXM1 in WI-38 cells.
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In male breast cancer patients high forkhead box protein M1 (FOXM) expression is significantly associated with disease free survival (DFS). Median progression free survival under chemotherapy or Tamoxifen hormone therapy is shorter for the High FOXM1 expression group. High FOXM1 expression is significantly associated with chemotherapy and endocrine resistance.
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High FoxM1 expression is associated with the development of prostate cancer.
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FOXM1 promotes proliferation in human hepatocellular carcinoma cells by transcriptional activation of CCNB1.
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Upregulation of FOXM1 in a subset of relapsed myeloma results in poor outcome.
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We first reported that the FOMX1 pathway is the most upregulated and the PPARalpha pathway is the most downregulated pathway in Triple Negative Breast Cancers (TNBCs). These two pathways could be simultaneously targeted in further studies. Also the pathway classifier we performed in this study provided insight into the TNBC heterogeneity.
