scholarly journals Characterization of a new B-ALL cell line with constitutional defect of the Notch signaling pathway

Oncotarget ◽  
2018 ◽  
Vol 9 (26) ◽  
pp. 18341-18350 ◽  
Author(s):  
Paul Takam Kamga ◽  
Giada Dal Collo ◽  
Giulio Bassi ◽  
Martina Midolo ◽  
Massimo Delledonne ◽  
...  
Keyword(s):  
Notch Signaling ◽  
Cell Line ◽  
Signaling Pathway ◽  
Notch Signaling Pathway

Structural and Functional Characterization of the NHR1 Domain of the Drosophila Neuralized E3 Ligase in the Notch Signaling Pathway

2009 ◽  
Vol 393 (2) ◽  
pp. 478-495 ◽  
Author(s):  
Fahu He ◽  
Kohei Saito ◽  
Naohiro Kobayashi ◽  
Takushi Harada ◽  
Satoru Watanabe ◽  
...  
Keyword(s):  
Notch Signaling ◽  
Signaling Pathway ◽  
Functional Characterization ◽  
E3 Ligase ◽  
Notch Signaling Pathway

scholarly journals Transcriptional characterization of the notch signaling pathway in rodent multipotent adult progenitor cells

2007 ◽  
Vol 13 (4) ◽  
pp. 302-310 ◽  
Author(s):  
Melinda Hajdu ◽  
Aernout Luttun ◽  
Beatriz Pelacho ◽  
Terry C Burns ◽  
Lucas Chase ◽  
...  
Keyword(s):  
Notch Signaling ◽  
Progenitor Cells ◽  
Signaling Pathway ◽  
Notch Signaling Pathway ◽  
Multipotent Adult Progenitor Cells

scholarly journals Characterization of the Stem Cell Fraction in Pancreatobiliary Carcinomas: The Notch Signaling Pathway as a Potential Therapeutic Target

2018 ◽  
Vol 09 (06) ◽  
pp. 480-502
Author(s):  
Elisabeth Seidel ◽  
Cynthia de Carvalho Fischer ◽  
Christopher Neumann ◽  
Anja Reutzel-Selke ◽  
Andreas Andreou ◽  
...  
Keyword(s):  
Stem Cell ◽  
Notch Signaling ◽  
Signaling Pathway ◽  
Therapeutic Target ◽  
Notch Signaling Pathway ◽  
Cell Fraction ◽  
Potential Therapeutic Target

Establishment of Dental Epithelial Cell Line (HAT-7) and the Cell Differentiation Dependent on Notch Signaling Pathway

2002 ◽  
Vol 43 (2) ◽  
pp. 409-412 ◽  
Author(s):  
Shintaro Kawano ◽  
Takahiko Morotomi ◽  
Takashi Toyono ◽  
Norifumi Nakamura ◽  
Takashi Uchida ◽  
...  
Keyword(s):  
Cell Differentiation ◽  
Epithelial Cell ◽  
Notch Signaling ◽  
Cell Line ◽  
Signaling Pathway ◽  
Notch Signaling Pathway ◽  
Epithelial Cell Line

scholarly journals Arsenic trioxide inhibits the proliferation of myeloma cell line through notch signaling pathway

2013 ◽  
Vol 13 (1) ◽  
pp. 25 ◽  
Author(s):  
Jiasheng Hu ◽  
Xiao Huang ◽  
Xiuli Hong ◽  
Quanyi Lu ◽  
Xiongpeng Zhu
Keyword(s):  
Notch Signaling ◽  
Cell Line ◽  
Arsenic Trioxide ◽  
Signaling Pathway ◽  
Myeloma Cell ◽  
Notch Signaling Pathway ◽  
Myeloma Cell Line

scholarly journals Sensitivity of non-small cell lung cancer to erlotinib is regulated by the Notch/miR-223/FBXW7 pathway

2017 ◽  
Vol 37 (3) ◽  
Author(s):  
Haiwei Zhang ◽  
Fanglin Chen ◽  
Yongpeng He ◽  
Lin Yi ◽  
Chuang Ge ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Growth Factor ◽  
Small Cell Lung Cancer ◽  
Notch Signaling ◽  
Cell Line ◽  
Signaling Pathway ◽  
Notch Signaling Pathway ◽  
Small Cell ◽  
Cell Resistance ◽  
Small Cell Lung

Recent evidence supports a role for microRNA-223 (miR-223) in modulating tumor cell sensitivity to chemotherapeutic drugs; however, its role in cellular resistance to the effects of epidermal growth factor receptor tyrosine kinase inhibitors (EGFR-TKIs) used in treatment of non-small cell lung cancer (NSCLC) remains to be elucidated. The levels of miR-223 in parental cell line (HCC827) and erlotinib resistant HCC827 cell line (HCC827/ER) were detected by qRT-PCR. HCC827/ER cells were treated with MK-2206 to block the Akt signaling pathway or RO4929097 to block the Notch signaling pathway, and then transfected with an miR-223 inhibitor or interference expression plasmid of F-Box/WD repeat-containing protein 7 (FBXW7) or insulin-like growth factor 1 receptor (IGF1R). HCC827 cells were transfected with miR-223 mimics. Next, CCK-8, colony formation, and flow cytometric apoptosis assays were used to assess cell resistance to erlotinib. When compared with its expression in HCC827 cells, miR-223 expression was significantly up-regulated in HCC827/ER cells. Blocking either the Akt or Notch signaling pathway and reducing miR-223 expression resulted in decreased resistance in HCC827/ER cells. Conversely, increasing miR-223 expression induced cell resistance to erlotinib in HCC827 cells. miR-223 enhanced resistance to erlotinib by down-regulating FBXW7 expression. Reducing FBXW7 expression lowered resistance to erlotinib in HCC827/ER cells, while interference with expression of IGF1R produced no significant effect. This study demonstrated that NSCLC cells can up-regulate their levels of miR-223 expression via the Akt and Notch signaling pathways. miR-223 may serve as an important regulator of erlotinib sensitivity in NSCLC cells by targeting FBXW7.

scholarly journals LncRNA NEAT1 mediates progression of oral squamous cell carcinoma via VEGF-A and Notch signaling pathway

2020 ◽  
Vol 18 (1) ◽  
Author(s):  
Ke He ◽  
Zhi-Bin Zhu ◽  
Rui Shu ◽  
Ai Hong
Keyword(s):  
Squamous Cell Carcinoma ◽  
Oral Squamous Cell Carcinoma ◽  
Notch Signaling ◽  
Cell Carcinoma ◽  
Cell Line ◽  
Signaling Pathway ◽  
Cell Lines ◽  
Squamous Cell ◽  
Notch Signaling Pathway ◽  
Lncrna Neat1

Abstract Background lncRNAs and VEGF have been shown to have close connections with oral squamous cell carcinoma (OSCC). We explored the interaction between lncRNA NEAT1 and VEGF-A in OSCC. Methods RT-qPCR was implemented to measure levels of lncRNA NEAT1 and VEGF-A in OSCC cell lines and normal cell lines. Cell functions then were checked after regulating the expressions of lncRNA NEAT1 and VEGF-A separately. Cell viabilities were examined with CCK-8 and apoptosis rate was checked with flow cytometry. Meanwhile, EMT-related genes E-cadherin, N-cadherin, Vimentin, and Snail and Notch signaling genes Notch1, Notch2, and Jagged were evaluated by RT-qPCR. IMR-1 was applied for impeding Notch signaling pathway. Later, cell viabilities, apoptosis, and EMT were assessed. Results Expressions of lncRNA NEAT1 and VEGF-A were both increased significantly in OSCC cell lines especially in TSCC1 cell line. Suppression of lncNRA NEAT1 was associated with lower cell viabilities and EMT and higher apoptosis rate in the TSCC1 cell line. Meanwhile, knockdown of VEGF-A significantly repressed cell viabilities and EMT in the TSCC1 cell line. Magnifying functions of inhibited lncRNA NEAT1 Notch signaling pathway was obviously activated with overexpressions of lncRNA NEAT1 and VEGF-A. Adding IMR-1 significantly downregulated cell viabilities and EMT and sharply increased apoptosis in the context of lncRNA NEAT1 and VEGF-A overexpression. Conclusion LncRNA NEAT1 may upregulate proliferation and EMT and repress apoptosis through activating VEGF-A and Notch signaling pathway in vitro, suggesting an underlying regulatory factor in OSCC. Nevertheless, further research is necessary to gain a greater understanding of lncRNA NEAT1 and connections with VEGF-A in vivo and in clinical study.

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