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FUBP1 regulates the oncogene KIT by binding to its enhancer, and its promoter, and by interacting with RUNX1.
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FUBP1 promotes tumor cell proliferation and migration and regulates the cancer cell immunity by increasing the PD-L1 expression mediated by Myc in pancreatic cancer cells.
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High FUBP1 expression is associated with low Chemosensitivity to Adriamycin in Gastric Cancer.
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Low FUBP1 expression is associated with adenovirus infection.
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These results suggest that the interference with the FUBP1/FUSE interaction as a further molecular mechanism that, in addition to the inactivation of TOP1, may contribute to the therapeutic potential of camptothecin/SN-38.
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The findings demonstrate an association between FUBP1 levels and chordoma progression and prognosis, suggesting that FUBP1 can be used as a biomarker and a potential therapeutic target.
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we identified cyclin J and far upstream element-binding protein 1 (FUBP1) as novel miR-16 targets, which mediate miR-16 antiproliferative effects.
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FUBP1 acts as a potential oncogene in clear cell renal cell carcinoma (ccRCC) and may be considered as a novel biomarker or an attractive treatment target of ccRCC.
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FBP1 expression in Bcell lymphoma was also associated with poor survival outcomes. Functionally, small interfering RNAmediated silencing of FBP1 was able to inhibit the proliferation of Bcell lymphoma cells, resulting in G0/G1 phase cell cycle arrest.
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FUBP1 may potentially stimulate c-Myc expression in ESCC and its expression may promote esophageal squamous cell carcinoma progression.
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With the advent of large-scale genome sequencing technology, molecular genetic alterations in FUBP1 promoter have now been identified in the majority of oligodendrogliomas
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direct connection between the cellular PI3K/AKT/mTOR signaling pathway, frequently activated in human hepatocarcinogenesis, and the enrichment of oncogenic transcription factors of the FBP family
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Concomitant overexpression of far upstream element (FUSE) binding protein (FBP) interacting repressor (FIR) and its splice variants induce migration and invasion of non-small cell lung cancer cells.
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FBP1 promotes hepatitis C virus eplication by inhibiting p53 expression.
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High FBP1 expression was observed in glioma.
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Apoptosis-mediated cleavage of FBP1 and its decreased expression in epithelial cells induces cell cycle arrest, which may play an important role in colonic epithelial disruption in colitis.
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We conclude that absent CIC and FUBP1 expressions are potential markers of shorter time to recurrence in oligodendroglial tumors.
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These findings are the first report describing the regulation of alternative splicing of MDM2 mediated by the oncogenic factor FUBP1.
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The data indicates an association between FUBP1 expression and proliferation in gliomas.
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FUBP1 expression differs among gastric tissues; there is a correlation between overall survival rates and age, sex, lymph node metastasis, and distant metastasis.
