Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
JNK1 stress signaling is hyper-activated in high breast density and the tumor stroma: connecting fibrosis, inflammation, and stemness for cancer prevention.
|
24434780 |
2014 |
Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
JNK suppresses tumor formation via a gene-expression program mediated by ATF2.
|
25456131 |
2014 |
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
JNK1 deletion suppressed the increase of diethylnitrosamine-induced tumor number in FXR(-/-) mice.
|
25496033 |
2015 |
Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
JNK drives the transcriptional induction of mitogenic molecules, matrix metalloproteases and systemic signals that lead to tumor growth, tissue invasiveness and malignancy.
|
29451063 |
2018 |
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
A JNK1 inhibitor also increased the latency period and decreased growth of MMTV-neu tumors by induction of apoptosis.
|
20944115 |
2010 |
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Akt-S6K1 inhibition and JNK activation were observed in ABC294640-treated tumors.
|
29428730 |
2018 |
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
An analysis of nine pancreatic cancer tissues revealed JNK activation in all tumor samples and ERK activation in three tumor samples.
|
12185592 |
2002 |
Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
Anti-miR-21 decreased protein expression of the tumour cell invasion mediators MAP4K1 and JNK, which are also known to be negatively regulated by PDCD4, and down-regulated integrin protein that is essential for MB leptomeningeal dissemination.
|
21775132 |
2011 |
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
ANXA3/JNK Signaling Promotes Self-Renewal and Tumor Growth, and Its Blockade Provides a Therapeutic Target for Hepatocellular Carcinoma.
|
26095609 |
2015 |
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
c-Jun N-terminal kinase in pancreatic tumor stroma augments tumor development in mice.
|
28837246 |
2017 |
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Collectively, ω-HUA-induced intracellular ROS generation induced breast cancer cell apoptosis through JNK and p38 signaling pathway activation, resulting in tumor regression.
|
28681938 |
2018 |
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Combining <i>in vitro</i> and <i>in vivo</i> functional analyses, we demonstrate that JNK inhibition both promotes tumor cell cytostasis and blocks activation of the proapoptotic protein Bax, thereby antagonizing chemotherapy-mediated cytotoxicity.
|
28611109 |
2017 |
Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
Compared with parental NU/Mock3, NU/Cap12, and NU/Cap32 cells: 1) induced higher tumor angiogenesis than NU/Mock3 cells accompanied by infiltration of tumor-associated macrophages in mouse dorsal air sac assay and Matrigel plug assay; 2) showed much higher expression of CXC chemokines, MMP-1, and the potent angiogenic factor VEGF-A; 3) increased the expression of the representative inflammatory cytokine, IL-1α; 4) augmented JNK phosphorylation and nuclear expression of activator protein 1 (AP-1).
|
23846687 |
2013 |
Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
Consistent with this, PPI inhibited tumor growth, protein expression levels of p65, DNMT1 and EZH2, and increased phosphorylation of SAPK/JNK in vivo.
|
27421653 |
2016 |
Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
Decreased p-JNK1/2 expression in cancer tissues was observed in 48.5% of breast infiltrating ductal carcinoma (IDC) cases and was correlated significantly with the increased tumor grade and the decreased age at diagnosis (p = 0.030 and 0.029).
|
16381010 |
2006 |
Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
Diallyl trisulfide suppresses tumor growth through the attenuation of Nrf2/Akt and activation of p38/JNK and potentiates cisplatin efficacy in gastric cancer treatment.
|
28344324 |
2017 |
Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
DUSP4 (MKP-2), a member of the mitogen-activated protein kinase phosphatase (MKP) family and potential tumor suppressor, negatively regulates the MAPKs (mitogen-activated protein kinases) ERK, p38 and JNK.
|
22965873 |
2013 |
Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
Ex vivo tumor analysis indicated significant molecular activity such as changes in the level of phosphoproteins JNK, Akt, and inflammation markers IL-6 and IFN-γ.
|
28135100 |
2017 |
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Forkhead transcription factor (Foxo3a) is a downstream effector of JNK-induced tumor suppression.
|
28099944 |
2017 |
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Further, loss of PTK7 activated the MKK7-JNK stress response pathway and impaired tumor growth in xenotransplantation assays.
|
24654231 |
2014 |
Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
Further, lysosomal cysteine peptidases modify growth factors and receptors involved in tyrosine kinase dependent pathways such as MAPK, Akt and JNK, thus representing key signaling tools for the activation of tumor cell growth and proliferation.
|
26255843 |
2015 |
Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
Furthermore, a xenograft assay showed that CT significantly inhibited MKN-45 cell-induced tumor growth <i>in vivo</i> by increasing expression of pro-apoptotic proteins (p-JNK, p-38 and cleaved-caspase-3) and reducing expression of anti-apoptotic proteins (p-ERK and p-STAT3) without adverse effects on nude mice weight.
|
29383168 |
2017 |
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Furthermore, A549 cells either pre-treated with SP600125 or transiently transfected with siRNAs against the JNK genes in vitro showed substantially reduced ability to initiate tumor formation upon implantation into nude mice, implying that the cell intrinsic JNK activity of A549 cells is essential for the maintenance of their tumor-initiating capacity.
|
23912840 |
2013 |
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Furthermore, restoration of JNK1 in ARMS reestablished a tumor-suppressive function for ILK.
|
19478459 |
2009 |
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Grnd localizes to the subapical membrane domain with the cell polarity determinant Crumbs (Crb) and couples Crb-induced loss of polarity with JNK activation and neoplastic growth through physical interaction with Veli (also known as Lin-7).
|
25874673 |
2015 |