|
KMID : 1161520170210030190
|
|
Animal Cells and Systems
2017 Volume.21 No. 3 p.190 ~ p.198
|
|
|
Differences in the starvation-induced autophagy response in MDA-MB-231 and MCF-7 breast cancer cells
|
|
Zhu Wanyun
Qu Hao
Xu Kaixiang
Jia Baoyu
Li Haifeng
Du Yimin
Liu Guangming
Wei Hong-Jiang
Zhao Hong-Ye
|
|
|
Abstract
|
|
|
|
Breast cancer is a heterogeneous disease with distinct subtypes that have made targeted therapy of breast cancer challenging. Previous studies have demonstrated that an altered autophagy capacity can influence the development of breast cancer. However, the molecular differences in starvation-induced autophagic responses in MDA-MB-231 and MCF-7 cells have not been fully elucidated. In this study, we found that an increase of LC3B-II protein expression level and a decrease of the p62 protein expression level in both cells treated by Earle’s balanced salt solution. Meanwhile, we observed an increase of autophagosome using transmission electron microscopy and an enhancement in the green fluorescence intensity of LC3B protein by confocal microscopy. Furthermore, we detected the expression of 13 autophagy-related (ATG) genes and 11 autophagy signaling pathway-related genes using qPCR. Among 13 ATG genes, we found that 6 genes were up-regulated in treated MDA-MB-231 cells, while 4 genes were up-regulated and 1 gene was down-regulated in treated MCF-7 cells. In addition, among 11 autophagy signaling pathway-related genes, 7 genes were up-regulated in treated MDA-MB-231 cells, while 5 genes were up-regulated and 1 gene was down-regulated in treated MCF-7 cells. These findings suggest that the autophagic response to starvation was different in the two treated cell lines, which will contribute to further study on the molecular mechanism of starvation-induced autophagy and improve the targeted therapy of breast cancer.
|
|
|
KEYWORD
|
|
|
MDA-MB-231, MCF-7, starvation, autophagy-related genes, autophagy signaling pathway-related genes
|
|
|
FullTexts / Linksout information
|
|
|
|
|
|
Listed journal information
|
|
 
|
|