Carcinogenesis
|
0.100 |
AlteredExpression
|
phenotype |
BEFREE |
Besides, PYCR1 expression was negatively regulated by miR-488, and up-regulation of miR-488 significantly inhibited cell proliferation and tumorigenesis and increased cell apoptosis, and decreased p38 expression and its nuclear accumulation, whereas up-regulation of PYCR1 rescued these results induced by miR-488 over-expression.
|
30605882 |
2019 |
Carcinogenesis
|
0.100 |
Biomarker
|
phenotype |
BEFREE |
Ablation of p38 in Becn1ΔM mice prevented neutrophil inflammation and B cell tumorigenesis.
|
31503548 |
2019 |
Carcinogenesis
|
0.100 |
Biomarker
|
phenotype |
BEFREE |
Correction: Inhibition of p38 MAPK Signaling Augments Skin Tumorigenesis via NOX2 Driven ROS Generation.
|
28196147 |
2019 |
Carcinogenesis
|
0.100 |
Biomarker
|
phenotype |
BEFREE |
Activation of ERK and JNK promotes tumorigenesis; whereas, escalation of p38 inhibits carcinogenesis.
|
31075266 |
2019 |
Carcinogenesis
|
0.100 |
Biomarker
|
phenotype |
BEFREE |
Our results suggested that WAVE3 may be pivotal in ovarian cancer cell motility, invasion and oncogenesis, which might be related with MMPs production and p38 MAPK pathway.
|
28476025 |
2017 |
Carcinogenesis
|
0.100 |
AlteredExpression
|
phenotype |
BEFREE |
Polymeric black tea polyphenols (PBPs) inhibit benzo(a)pyrene and 4-(methylnitrosamino)-1-(3-pyridyl)-1- butanone-induced lung carcinogenesis potentially through down-regulation of p38 and Akt phosphorylation in A/J mice.
|
27377358 |
2017 |
Carcinogenesis
|
0.100 |
Biomarker
|
phenotype |
BEFREE |
Mechanistically, activation of TPL2 downstream signaling pathways such as MEK/ERK MAPK, mTOR, NF-κB, and p38 MAPK leads to TPL2-mediated cell transformation in immortalized human keratinocytes and tumorigenesis in mice.
|
27503930 |
2016 |
Carcinogenesis
|
0.100 |
AlteredExpression
|
phenotype |
BEFREE |
Inhibition of EGFR reduces p38 MAPK, resulting in decreased expression of hypoxia-inducible factor-1α, metalloproteinase 1, and VEGF, leading to suppressions of angiogenesis and tumorigenesis.
|
27226640 |
2016 |
Carcinogenesis
|
0.100 |
GeneticVariation
|
phenotype |
BEFREE |
Systemic down-regulation of p38MAPK signaling in a knock-in model with substitution of activating Tyr182 to phenylalanine or conditional ablation of p38 in fibroblasts has a significant tumor-suppressive effect on K-ras lung tumorigenesis.
|
28007785 |
2016 |
Carcinogenesis
|
0.100 |
AlteredExpression
|
phenotype |
BEFREE |
NOB1 and p38 MAPK expression had significant positive correlation with carcinogenesis, tumor progression and patient survival.
|
24228091 |
2013 |
Carcinogenesis
|
0.100 |
Biomarker
|
phenotype |
BEFREE |
Here, we show for the first time that the simultaneous knockdown in vitro, compared with the single knockdown of HER2 and PTK6, in particular in the trastuzumab-resistant JIMT-1 cells, leads to a significantly decreased phosphorylation of crucial signaling proteins: mitogen-activated protein kinase 1/3 (MAPK 1/3, ERK 1/2) and p38 MAPK, and (phosphatase and tensin homologue deleted on chromosome ten) PTEN that are involved in tumorigenesis.
|
23364537 |
2013 |
Carcinogenesis
|
0.100 |
Biomarker
|
phenotype |
BEFREE |
LY2228820 dimesylate is a highly selective small molecule inhibitor of p38α and p38β mitogen-activated protein kinases (MAPKs) that is currently under clinical investigation for human malignancies. p38 MAPK is implicated in a wide range of biological processes, in particular those that support tumorigenesis.
|
23335506 |
2013 |
Carcinogenesis
|
0.100 |
AlteredExpression
|
phenotype |
BEFREE |
Our findings suggest that SRC, c-MET and CRK play a key role in gastric carcinogenesis by modulating CagA signal transductions and interaction between CRK gene and phytoestrogens modify gastric cancer risk.
|
22383989 |
2012 |
Carcinogenesis
|
0.100 |
AlteredExpression
|
phenotype |
BEFREE |
This is in direct contrast to carcinoma cells in which the activity of the two kinases appears to be mutually exclusive; high level of p38 activity inhibits, through a negative feedback, ERK activity and prevents tumorigenesis.
|
18983537 |
2009 |
Carcinogenesis
|
0.100 |
Biomarker
|
phenotype |
BEFREE |
Its association with such key molecules as topoisomerase IIalpha, p38 MAPK, and integrin beta1, has important clinical implications, including its potential ability to regulate tumor sensitivity to selected chemotherapies and to influence tumor migration/metastases and tumorigenesis.
|
17346218 |
2007 |
Carcinogenesis
|
0.100 |
Biomarker
|
phenotype |
BEFREE |
It is established that p38 MAPK can negatively regulate tumorigenesis, but the mechanism is incompletely understood.
|
17292820 |
2007 |
Carcinogenesis
|
0.100 |
AlteredExpression
|
phenotype |
BEFREE |
Here we show that a subtle activation of p38 MAPK is sufficient to suppress tumorigenesis as measured by the ability to form tumors when MKK6-inducible cells were explanted into nude mice.
|
15611662 |
2005 |
Carcinogenesis
|
0.100 |
Biomarker
|
phenotype |
BEFREE |
FACL4 is involved in the HCC tumorigenesis and both cAMP and p38 MAPK pathways are associated with the regulation of FACL4 in HCC.
|
15849811 |
2005 |
Carcinogenesis
|
0.100 |
Biomarker
|
phenotype |
BEFREE |
These data indicate that amplification and increased expression of the C3G gene may play some role in human lung carcinogenesis through derangement of the CRK-Rap1 signaling pathway.
|
15138850 |
2004 |