Triple Negative Breast Neoplasms
|
0.100 |
Biomarker
|
disease |
BEFREE |
Targeting Notch1/MVP pathway appears to have potential in overcoming chemoresistance in TNBC.
|
30336197 |
2019 |
Triple Negative Breast Neoplasms
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
Our studies demonstrated that SAHA and VPA might be considered as potential therapeutic agents in combination therapy with CDDP against TNBC with altered Notch1 activity.
|
31357442 |
2019 |
Triple Negative Breast Neoplasms
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
We further show that upregulation of NOTCH1 is necessary for TIC induction downstream of miR-106b-25 in both ER + and TNBC breast cancer cells, and that re-expression of NEDD4L is sufficient to reverse miR106b-25-mediated NOTCH1 upregulation and TIC induction.
|
29662198 |
2018 |
Triple Negative Breast Neoplasms
|
0.100 |
Biomarker
|
disease |
BEFREE |
Notch1 co-localizes with mitochondria in TNBC cells.
|
30564555 |
2018 |
Triple Negative Breast Neoplasms
|
0.100 |
Biomarker
|
disease |
BEFREE |
Notch1 was validated as the direct target gene of miR-3178, which was confirmed by the dual-luciferase reporter assay. miR-3178 decreased the expression of Notch1 and restoration of Notch1 expression attenuated the inhibitory effects of miR-3178 on cell proliferation, metastasis, and the EMT in TNBC. miR-3178 inhibited cell proliferation and metastasis by targeting Notch1 in TNBC, and the restoration of miR-3178 might be a potential therapeutic strategy for TNBC.
|
30333478 |
2018 |
Triple Negative Breast Neoplasms
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
Here, we demonstrated that hypoxia up-regulates both the levels of Orai1 and Notch1, and the increase in Orai1 is mediated by Notch1 signaling in TNBCs.
|
29307746 |
2018 |
Triple Negative Breast Neoplasms
|
0.100 |
Biomarker
|
disease |
BEFREE |
DEAE-Dextran coated paclitaxel nanoparticles act as multifunctional nano system for intranuclear delivery to triple negative breast cancer through VEGF and NOTCH1 inhibition.
|
29031923 |
2018 |
Triple Negative Breast Neoplasms
|
0.100 |
Biomarker
|
disease |
BEFREE |
Pursuant to our previous finding that HDAC8 regulates CSCs in triple-negative breast cancer (TNBC) cells by targeting Notch1 stability, we investigated related pathways and found HDAC3 to be mechanistically linked to CSC homeostasis by increasing β-catenin expression through the Akt/GSK3β pathway.
|
28923385 |
2017 |
Triple Negative Breast Neoplasms
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
We further demonstrated that both JNK1 and JNK2 regulated Notch1 transcription via activation of c-Jun and that the JNK/c-Jun signaling pathway promoted CSC phenotype through Notch1 signaling in TNBC.
|
27941886 |
2017 |
Triple Negative Breast Neoplasms
|
0.100 |
Biomarker
|
disease |
BEFREE |
Here, we report a signaling pathway involving BRD4 and the ligand/receptor pair Jagged1/Notch1 that sustains triple-negative breast cancer migration and invasion.
|
27651315 |
2016 |
Triple Negative Breast Neoplasms
|
0.100 |
Biomarker
|
disease |
BEFREE |
Targeting of miR9/NOTCH1 interaction reduces metastatic behavior in triple-negative breast cancer.
|
25963903 |
2015 |
Triple Negative Breast Neoplasms
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
NOTCH1 and NOTCH2 rearrangements leading to constitutive receptor activation were confined to triple-negative breast cancers (TNBC; 6 of 66 tumors).
|
25104330 |
2014 |
Triple Negative Breast Neoplasms
|
0.100 |
Biomarker
|
disease |
BEFREE |
Some of these markers are p53-induced miR-205, leptin receptor antagonist peptide, enhancer of zeste homolog 2 and Notch 1 pathway components, each of them could offer different mechanism for target therapy in TNBC.
|
23824643 |
2013 |