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• W2897411332 abstract "The ubiquitin ligase F‐box and WD repeat domain‐containing 7 ( FBXW 7) is responsible for degrading diverse oncoproteins and is considered a tumor suppressor in many human cancers. Inhibiting FBXW 7 enhances the malignant potential of several cancers. In this study, we aimed to investigate the role of FBXW 7 in cholangiocarcinoma. We found that FBXW 7 expression was associated with clinicopathological outcomes in cholangiocarcinoma patients. Both disease‐free and overall survival were significantly worse in the low‐ FBXW 7 group than in the high‐ FBXW 7 group ( P = .001 and P < .001, respectively). Multivariate analysis with the Cox proportional hazards model indicated that FBXW 7 was the most important independent prognostic factor for disease‐free ( P = .006) and overall ( P = .0004) survival. We also showed that the two FBXW 7 substrates, NOTCH 1 and myeloid cell leukemia sequence 1 ( MCL 1), regulate cholangiocarcinoma progression. Depletion of FBXW 7 resulted in NOTCH 1 accumulation and increased cholangiocarcinoma cell migration and self‐renewal. Interestingly, when cells were stimulated with cis‐diamminedichloridoplatinum( II ) (cisplatin), FBXW 7 suppression induced MCL 1 upregulation, which reduced the sensitivity of cholangiocarcinoma cells to apoptosis, indicating that FBXW 7‐mediated ubiquitylation is context‐dependent. These results indicate that FBXW 7 modulates the malignant potential of cholangiocarcinoma through independent regulation of NOTCH 1 and MCL 1." @default.
• W2897411332 created "2018-10-26" @default.
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• W2897411332 date "2018-11-05" @default.
• W2897411332 modified "2023-10-14" @default.
• W2897411332 title "<scp>FBXW</scp>7 modulates malignant potential and cisplatin‐induced apoptosis in cholangiocarcinoma through<scp>NOTCH</scp>1 and<scp>MCL</scp>1" @default.
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• W2897411332 doi "https://doi.org/10.1111/cas.13829" @default.
• W2897411332 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/6272118" @default.
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• W2897411332 hasPublicationYear "2018" @default.
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