melanoma
|
0.100 |
Biomarker
|
disease |
BEFREE |
In conclusion, our broad-in-depth work suggests that SHARPIN promotes melanoma development via p38 and JNK/c-Jun pathways through upregulation of Rap1 expression.
|
31401046 |
2020 |
melanoma
|
0.100 |
Biomarker
|
disease |
BEFREE |
Collectively, our data show that JNK2 activity is specifically required for melanoma cell proliferation, invasiveness, and BRAFi resistance and that this activity is most important in the context of JNK1 suppression, thus providing a compelling rationale for the development of JNK2 selective inhibitors as a potential therapy for the treatment of melanoma.
|
31063355 |
2019 |
melanoma
|
0.100 |
Biomarker
|
disease |
BEFREE |
Although the FDA has approved some JNK inhibitors for melanoma, the agency has not approved JNK inhibitors for ovarian cancer.
|
31639019 |
2019 |
melanoma
|
0.100 |
Biomarker
|
disease |
BEFREE |
VE-cadherin-mediated integrin signaling occurred through specific activation of SRC, ERK and JNK, including AKT in melanoma.
|
27966446 |
2017 |
melanoma
|
0.100 |
Biomarker
|
disease |
BEFREE |
MALT1 promotes melanoma progression through JNK/c-Jun signaling.
|
28759024 |
2017 |
melanoma
|
0.100 |
Biomarker
|
disease |
BEFREE |
Induction of MDA-9/syntenin in melanoma was found to occur in a thrombin-independent signaling pathway and involves the PAR-1/c-Src/Rho GTPases Rac1 and Cdc42/c-Jun N-terminal kinase axis resulting in the activation of paxillin, NF-κB, and matrix metalloproteinase-2 (MMP-2).
|
25505176 |
2015 |
melanoma
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
Systematic analysis of BRAF(V600E) melanomas reveals a role for JNK/c-Jun pathway in adaptive resistance to drug-induced apoptosis.
|
25814555 |
2015 |
melanoma
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
Synergistic cytotoxicity of radiation and oncolytic Lister strain vaccinia in (V600D/E)BRAF mutant melanoma depends on JNK and TNF-α signaling.
|
23624923 |
2014 |
melanoma
|
0.100 |
Biomarker
|
disease |
BEFREE |
By showing that down-regulation of CCL2-driven signals by SAHA and temozolomide via JNK contributes to reduce melanoma growth, we provide a rationale for the therapeutic advantage of the drug combination.
|
24980831 |
2014 |
melanoma
|
0.100 |
Biomarker
|
disease |
BEFREE |
Thus, restoration of CYLD and inhibition of JNK and β1-integrin function represent potential therapeutic strategies for treatment of malignant melanoma.
|
22832488 |
2013 |
melanoma
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
Furthermore, Pin1 inhibition also resulted in decreased phosphorylation of Akt and repressed expression of C-Jun N-terminal kinase and pro-matrix metalloproteinase 2, which were associated closely with the development of melanoma.
|
23067222 |
2013 |
melanoma
|
0.100 |
Biomarker
|
disease |
BEFREE |
Involvement of endoplasmic reticulum stress in Docetaxel-induced JNK-dependent apoptosis of human melanoma.
|
18989785 |
2008 |
melanoma
|
0.100 |
Biomarker
|
disease |
LHGDN |
Together, our findings demonstrate that JNK, and in particular the JNK1 isoform, support the growth of melanoma cells, by controlling either cell cycle progression or apoptosis depending on the cellular context.
|
18541008 |
2008 |
melanoma
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
Together, our findings demonstrate that MAPK-ERK and MAPK-JNK are regulators of CIITA transcription in melanoma, and pinpoint an AP-1-responsive site in the CIITA gene pIII.
|
17304627 |
2007 |