Breast Carcinoma
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
Our in vivo experiments also show that GL-V9 significantly inhibits the growth of human breast cancer due to activation of GSK-3β and inactivation of AKT.
|
31669347 |
2020 |
Breast Carcinoma
|
0.100 |
Biomarker
|
disease |
BEFREE |
We employed TWS119 to inactivate GSK-3β by phosphorylating Ser9 and explored its effect on breast cancer and NK cells.
|
31119045 |
2019 |
Breast Carcinoma
|
0.100 |
Biomarker
|
disease |
BEFREE |
Overexpression of novel lncRNA NLIPMT inhibits metastasis by reducing phosphorylated glycogen synthase kinase 3β in breast cancer.
|
30417392 |
2019 |
Breast Carcinoma
|
0.100 |
Biomarker
|
disease |
BEFREE |
Furthermore, GSK3β can regulate cell viability through the PTEN/PI3K/AKT signaling pathway and induce chemoresistance, serving as a valuable molecular strategy for breast cancer therapy.
|
31006103 |
2019 |
Breast Carcinoma
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
We found excessive GSK-3β expression in BC tissues, which was correlated with worse clinicopathological parameters and clinical outcome.
|
30037362 |
2019 |
Breast Carcinoma
|
0.100 |
Biomarker
|
disease |
BEFREE |
Together, our results show that TP53INP1 inhibits hypoxia-induced EMT and VM formation via the ROS/GSK-3β/Snail pathway in breast cancer, which offers new insights into breast cancer clinical therapy.
|
29655255 |
2018 |
Breast Carcinoma
|
0.100 |
Biomarker
|
disease |
BEFREE |
Nuclear GSK-3β expression was associated with HER-2 positive tumors (P=0.02) and non-triple negative breast carcinomas (P=0.0001), although nuclear GSK-3β was observed in some samples across all breast cancer subtypes.
|
30405781 |
2018 |
Breast Carcinoma
|
0.100 |
Biomarker
|
disease |
BEFREE |
In conclusion, the present study indicated that the identified DEGs and hub genes further our understanding of the molecular mechanisms underlying trastuzumab treatment in BC and highlighted GSK3B, which might be used as a molecular target for the treatment of BC.
|
30181805 |
2018 |
Breast Carcinoma
|
0.100 |
Biomarker
|
disease |
BEFREE |
Results from the in vivo and in vitro experiments both showed that fucoidan decreased the levels of p-PI3K, p-AKT and p-GSK-3β (Ser9) in breast cancer.
|
28810530 |
2017 |
Breast Carcinoma
|
0.100 |
Biomarker
|
disease |
BEFREE |
Furthermore, we found that overexpression of miR-1229 activated the Wnt/β-catenin signaling pathway in breast cancer by directly targeting the multiple important negative regulators of Wnt/β-catenin signaling, including adenomatous polyposis coli (APC), glycogen synthase kinase-3β (GSK-3β), and inhibitor of β-catenin and T cell factor (ICAT).
|
26992223 |
2016 |
Breast Carcinoma
|
0.100 |
Biomarker
|
disease |
BEFREE |
In summary, our findings demonstrated that miR-143 down-regulated its target ERK5, leading to the suppression of EMT induced by GSK-3β/Snail signaling of breast cancer.
|
26618772 |
2016 |
Breast Carcinoma
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
Inactivation of GSK3β as measured by its phosphorylation at Ser9 is positively correlated with higher level of H3K27 trimethylation in tumor tissues from breast cancer patients.
|
27494834 |
2016 |
Breast Carcinoma
|
0.100 |
Biomarker
|
disease |
BEFREE |
Interestingly, we observed increased phosphorylation of GSK-3β, NF-κB, and ERα only in MCF-7 cells, highlighting their role as potential targets in prevention of progression of breast cancer under a high-glucose and insulin condition.
|
23690508 |
2013 |
Breast Carcinoma
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
Our results indicate that AD-PTEN sensitization of breast cancer to LY294002 is achieved by increased GSK-3β activity, thus resulting in inhibition of the β-catenin signaling pathway.
|
22710837 |
2012 |
Breast Carcinoma
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
We suggest that analysis of both GSK3β and cyclin D1 expressions can be considered as a marker of good prognosis in early breast cancer.
|
22976805 |
2012 |
Breast Carcinoma
|
0.100 |
Biomarker
|
disease |
BEFREE |
Here, we report a comprehensive study of the contribution of genetic variation in six genes encoding the beta-catenin destruction complex (APC, AXIN1, AXIN2, CSNK1D, CSNK1E, and GSK3B) to breast cancer using a Mayo Clinic Breast Cancer Case-Control Study.
|
18708403 |
2008 |