Activation of TWIST1 by COL11A1 promotes chemoresistance and inhibits apoptosis in ovarian cancer cells by modulating NF-κB-mediated IKKβ expression
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Title
Activation of TWIST1 by COL11A1 promotes chemoresistance and inhibits apoptosis in ovarian cancer cells by modulating NF-κB-mediated IKKβ expression
Authors
Keywords
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Journal
INTERNATIONAL JOURNAL OF CANCER
Volume 141, Issue 11, Pages 2305-2317
Publisher
Wiley
Online
2017-08-17
DOI
10.1002/ijc.30932
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Related references
Note: Only part of the references are listed.- TWIST1 drives cisplatin resistance and cell survival in an ovarian cancer model, via upregulation of GAS6, L1CAM, and Akt signalling
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- Overexpression of the RNA-binding proteins Lin28B and IGF2BP3 (IMP3) is associated with chemoresistance and poor disease outcome in ovarian cancer
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- miR-186 regulation of Twist1 and ovarian cancer sensitivity to cisplatin
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- COL11A1 confers chemoresistance on ovarian cancer cells through the activation of Akt/c/EBPβ pathway and PDK1 stabilization
- (2015) Yi-Hui Wu et al. Oncotarget
- Overexpression of CHI3L1 is associated with chemoresistance and poor outcome of epithelial ovarian carcinoma
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- FOXM1 confers to epithelial-mesenchymal transition, stemness and chemoresistance in epithelial ovarian carcinoma cells
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- Role of the Human High-Affinity Copper Transporter in Copper Homeostasis Regulation and Cisplatin Sensitivity in Cancer Chemotherapy
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- Epithelial-Mesenchymal Transition Induced by TNF- Requires NF- B-Mediated Transcriptional Upregulation of Twist1
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- Programmed Cell Death Protein 4 Down-regulates Y-Box Binding Protein-1 Expression via a Direct Interaction with Twist1 to Suppress Cancer Cell Growth
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- Short interfering RNA directed against TWIST, a novel zinc finger transcription factor, increases A549 cell sensitivity to cisplatin via MAPK/mitochondrial pathway
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