@Article{096504018X15323394008784,
AUTHOR = {Lu Guo, Duankai Chen, Xing Yin, Qingfeng Shu},
TITLE = {GSK-3b Promotes Cell Migration and Inhibits Autophagy by Mediating  the AMPK Pathway in Breast Cancer},
JOURNAL = {Oncology Research},
VOLUME = {27},
YEAR = {2019},
NUMBER = {4},
PAGES = {487--494},
URL = {http://www.techscience.com/or/v27n4/48562},
ISSN = {1555-3906},
ABSTRACT = {GSK-3 is a versatile protein kinase participating in many reactions. Currently, there is insufficient 
understanding of its influence on breast cancer (BC). In order to explore its influence on migration and 
invasion in BC, we investigated its expression in BC cell lines using qRT-PCR and Western blot (WB). 
Immunohistochemistry (IHC) was used to examine the potential of GSK-3 to predict clinical outcome in 
BC patients. GSK-3 knockdown was achieved using an shRNA plasmid vector in T47D cells. Our research 
explored the biological reactions and downstream pathways involved. We found excessive GSK-3 expression in BC tissues, which was correlated with worse clinicopathological parameters and clinical outcome. 
Progression of BC was suppressed by GSK-3 knockdown. Furthermore, suppression of GSK-3 function 
led to a noticeable decrease in ATP generation, and this was associated with stimulation of AMP-activated 
protein kinase (AMPK) in T47D cells. Activation of AMPK, a typical sign of autophagy stimulation, was 
triggered after suppression of GSK-3 function, in parallel with increased generation of LC3 II. Our findings 
therefore indicate that GSK-3 participates in regulation of migration as well as stimulation of autophagy 
via mediating activation of the AMPK pathway. This suggests that GSK-3 has potential as a predictor of 
clinical outcome and as a target for BC therapy.},
DOI = {10.3727/096504018X15323394008784}
}