scholarly journals Inhibition of mitogen-activated protein kinase signaling pathway sensitizes breast cancer cells to endoplasmic reticulum stress-induced apoptosis

2016 ◽  
Vol 35 (4) ◽  
pp. 2113-2120 ◽  
Author(s):  
FEN YANG ◽  
XIAO YAN TANG ◽  
HAO LIU ◽  
ZHI WEN JIANG
Keyword(s):  
Breast Cancer ◽  
Endoplasmic Reticulum ◽  
Protein Kinase ◽  
Endoplasmic Reticulum Stress ◽  
Breast Cancer Cells ◽  
Mitogen Activated Protein Kinase ◽  
Mitogen Activated Protein ◽  
Induced Apoptosis ◽  
Protein Kinase Signaling ◽  
Kinase Signaling Pathway

The Effect of Wnt Family Member 5a Gene Silencing on the Proliferation of Achondroplasia Using a DNAzymes-CoOOH Nanocomposite

2021 ◽  
Vol 17 (7) ◽  
pp. 1426-1434
Author(s):  
Hairui Xie ◽  
Lili Zhou ◽  
Zhijiang Chen ◽  
Hong Zhao
Keyword(s):  
Endoplasmic Reticulum ◽  
Endoplasmic Reticulum Stress ◽  
Family Member ◽  
Interaction Analysis ◽  
Mitogen Activated Protein Kinase ◽  
Mitogen Activated Protein ◽  
Endoplasmic Reticulum Stress Pathway ◽  
Protein Kinase Signaling ◽  
Kinase Signaling Pathway

Achondroplasia is a kind of congenital dysplasia due to the defect of endochondral ossification. Achondroplasia is considered to be a protein folding disease leading to endoplasmic reticulum stress. Endoplasmic reticulum stress may lead to disease by affecting the function and survival state of chondrocytes, but the specific mechanism requires further study. In this study, bioinformatics methods, online database mining, screening of differentially expressed genes for pathway enrichment, and interaction analysis were conducted to detect the Wnt family member 5a (Wnt5a) gene. Additionally, we designed a novel DNAzymes-based nanocomposite that can simultaneously silence Wnt5a genes in chondrocytes. The nanocomposite was composed of amino-functionalized cobalt oxyhydroxide nanoflakes modified by DNAzymes that target the Wnt5a gene. Further, we conducted in vitro experiments to verify that Wnt5a can mediate the mitogen-activated protein kinase signaling pathway through the endoplasmic reticulum stress pathway to affect the proliferation of chondrocytes.

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