Blockade of Notch Signaling with Gamma-Secretase Inhibitors Induces Apoptosis in the Stem-Like Population of Breast Cancer Cells.

Author(s):  
K. Foreman ◽  
P. Grudzien ◽  
S. Lo ◽  
P. Robinson ◽  
K. Albain ◽  
...  
2020 ◽  
Vol 328 ◽  
pp. 109200
Author(s):  
Prem Prakash Kushwaha ◽  
Atul Kumar Singh ◽  
Mohd Shuaib ◽  
Kumari Sunita Prajapati ◽  
Pothabathula Seshu Vardhan ◽  
...  

2021 ◽  
Vol 11 (12) ◽  
pp. 2401-2406
Author(s):  
Jing Gao ◽  
Xiangchuan Liu ◽  
Huijuan Shi ◽  
Shugang Liu

Our study explores miR-150’s effect on the biological activity of breast cancer cells and its correlation with Notch signaling. Human breast cancer cells MCF-7 were divided into WZ group (MCF-7 cells); KZ group (transfected with miR-150-NC); and group II (transfected with miR-150inhibitor) followed by analysis of miR-150 expressio,n cell replication, apoptosis, invasion, migration ability and Notch1 and Notch3 expression by qRT-PCR, cloning, Hoechst33258 fluorescent staining, Transwell chamber, cell scratch test, dual luciferase report and Western blot. Lowest miR-150 expression in MCF-7 cells indicated a successful transfection (P < 0.05). Compared with KZ and WZ groups, Notch1 and Notch3 mRNA levels in group II were decreased (P <0.05); and the number of cell clones in group II was reduced (P <0.05) without difference between WZ and KZ group (P >0.05); miR-150 inhibitor reduced Notch1 and Notch3 expression (P <0.05). The fluorescence intensity of MCF-7 cells in group II was highest among three groups (P <0.05). The number of cell invasion and migration as well as Notch1 and Notch 3 expression in group II was reduced (P <0.05) without difference between group KZ and WZ (P >0.05). miR-150 expression is increased in MCF-7 cells. The miR-150 inhibitor can inhibit cell apoptosis, migration and other biological behaviors, which is related to target Notch signaling pathway.


2020 ◽  
Vol 128 ◽  
pp. 110302 ◽  
Author(s):  
Azizah S. Bawadood ◽  
Fahad A. Al-Abbasi ◽  
Firoz Anwar ◽  
Ali M. El-Halawany ◽  
Ahmed M. Al-Abd

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