Carcinogenesis
|
0.100 |
Biomarker
|
phenotype |
BEFREE |
A human endogenous retrovirus-derived gene that can contribute to oncogenesis by activating the ERK pathway and inducing migration and invasion.
|
28651004 |
2017 |
Carcinogenesis
|
0.100 |
GeneticVariation
|
phenotype |
BEFREE |
Aberrant signaling of the Ras-Raf-MEK-ERK (MAP kinase) pathway driven by the mutant kinase BRAF(V600E), as a result of the BRAF(T1799A) mutation, plays a fundamental role in thyroid tumorigenesis.
|
21185263 |
2011 |
Carcinogenesis
|
0.100 |
AlteredExpression
|
phenotype |
BEFREE |
Activation of ERK and JNK promotes tumorigenesis; whereas, escalation of p38 inhibits carcinogenesis.
|
31075266 |
2019 |
Carcinogenesis
|
0.100 |
AlteredExpression
|
phenotype |
BEFREE |
Altogether, these findings establish RanBPM as a novel inhibitor of the ERK pathway through an interaction with the c-Raf complex and a regulation of c-Raf stability, and provide evidence that RanBPM loss of expression results in constitutive activation of the ERK pathway and promotes cellular events leading to cellular transformation and tumorigenesis.
|
23118896 |
2012 |
Carcinogenesis
|
0.100 |
Biomarker
|
phenotype |
BEFREE |
As nuclear translocation of ERK is a key step in carcinogenesis, inhibition of this event is proposed as a novel anticancer mechanism for biased β-blockers such as carvedilol.
|
29626349 |
2018 |
Carcinogenesis
|
0.100 |
Biomarker
|
phenotype |
BEFREE |
At last, up-regulation of miR-206 suppressed expression of <i>p</i>-AKT and <i>p</i>-ERK by targetting TM4SF1 in PGE2-induced cells.Our results provide further evidence that miR-206 has a protective effect on PGE2-induced colon carcinogenesis.
|
30135139 |
2018 |
Carcinogenesis
|
0.100 |
Biomarker
|
phenotype |
BEFREE |
Because TGF-β is known to activate the MAPK/ERK pathway through direct phosphorylation of the adaptor protein ShcA and MAPK/ERK signaling is pivotal to tumor progression, we investigated whether ShcA contributed to mp53-induced ERK inhibition and the conversion of the role of TGF-β during carcinogenesis.
|
22039050 |
2011 |
Carcinogenesis
|
0.100 |
Biomarker
|
phenotype |
BEFREE |
BRAF plays an indispensable role in activating the MEK/ERK pathway to drive tumorigenesis.
|
31015455 |
2019 |
Carcinogenesis
|
0.100 |
GeneticVariation
|
phenotype |
BEFREE |
CKAP2 Promotes Ovarian Cancer Proliferation and Tumorigenesis Through the FAK-ERK Pathway.
|
28933561 |
2017 |
Carcinogenesis
|
0.100 |
Biomarker
|
phenotype |
BEFREE |
Collectively, the present results suggested that the inhibitory effects of afatinib on EMT and tumorigenesis may be associated with the ERK‑VEGF/MMP9 signaling pathway.
|
31432165 |
2019 |
Carcinogenesis
|
0.100 |
Biomarker
|
phenotype |
BEFREE |
Constitutive activation of the Ras-ERK/MAPK signaling pathway often leads to promotion of abnormal cell growth and tumorigenesis.
|
21688267 |
2012 |
Carcinogenesis
|
0.100 |
Biomarker
|
phenotype |
BEFREE |
Deregulation of its expression or localization leads to epithelial defects and tumorigenesis in part as a consequence of its repressive role on several signaling pathways including AKT, ERK, and HIPPO.
|
31513346 |
2019 |
Carcinogenesis
|
0.100 |
GeneticVariation
|
phenotype |
BEFREE |
Disruption of the Raf/MEK/ERK (MAPK) kinase pathway-either through RAS or BRAF mutation-was detected in 27% of all UC-related cancers and thus plays an important role in UC-related carcinogenesis.
|
15704157 |
2005 |
Carcinogenesis
|
0.100 |
GeneticVariation
|
phenotype |
BEFREE |
Disruption of the Raf/MEK/ERK (MAPK) kinase pathway, either by RAS or BRAF mutation, was detected in approximately 62% of all CC and is therefore one of the most frequent defects in cholangiocellular carcinogenesis.
|
12692057 |
2003 |
Carcinogenesis
|
0.100 |
Biomarker
|
phenotype |
BEFREE |
Dysregulated activation of Ras or its downstream effectors such as mitogen-activated protein kinase kinase and ERK has been shown to play a critical role in tumorigenesis of many cancer types.
|
12591721 |
2003 |
Carcinogenesis
|
0.100 |
AlteredExpression
|
phenotype |
BEFREE |
Epithelial EphB2 expression was shown at all stages of colorectal tumorigenesis, including the base of all normal crypts, 77% of adenomas, 82% of primary cancers, and 64% of metastases.
|
16033834 |
2005 |
Carcinogenesis
|
0.100 |
Biomarker
|
phenotype |
BEFREE |
Expression of the SH3PXD2A-HTRA1 fusion resulted in elevated phosphorylated ERK, increased proliferation, increased invasion and in vivo tumorigenesis.
|
27723760 |
2016 |
Carcinogenesis
|
0.100 |
Biomarker
|
phenotype |
BEFREE |
FGFR2 regulates Mre11 expression and double-strand break repair via the MEK-ERK-POU1F1 pathway in breast tumorigenesis.
|
25788520 |
2015 |
Carcinogenesis
|
0.100 |
Biomarker
|
phenotype |
BEFREE |
Frequent deletion and decreased expression of EphB2 protein suggested it as a negative biomarker for gastric carcinogenesis and a potential predictor of the outcome of patients with gastric cancer.
|
20238226 |
2011 |
Carcinogenesis
|
0.100 |
Biomarker
|
phenotype |
BEFREE |
Furthermore, HeLa cells with exogenous EphB2 exhibited a stem cell-like state that promoted tumorsphere formation in vitro and exhibited tumorigenesis potential in vivo (P < .05), whereas EphB2 silencing in C33A cells inhibited these stem cell properties (P < .05).
|
24439224 |
2014 |
Carcinogenesis
|
0.100 |
GeneticVariation
|
phenotype |
BEFREE |
Furthermore, the phospho-deficient T205A FBW7 mutant is resistant to ERK activation and could significantly suppress pancreatic cancer cell proliferation and tumorigenesis.
|
25753158 |
2015 |
Carcinogenesis
|
0.100 |
Biomarker
|
phenotype |
BEFREE |
Furthermore, we show that the WW domain is not required for ERK-IQGAP1 binding, and contributes little or no binding energy to this interaction, challenging previous models of how WW-based peptides might inhibit tumorigenesis.
|
28396345 |
2017 |
Carcinogenesis
|
0.100 |
AlteredExpression
|
phenotype |
BEFREE |
Good correlation between H-ras expression levels and those of the upstream and downstream signaling proteins of EGFR, MEK and ERK was found, suggesting that H-ras may play a significant role in carcinogenesis of colorectal cancer.
|
11605075 |
2001 |
Carcinogenesis
|
0.100 |
AlteredExpression
|
phenotype |
BEFREE |
Here, we show that SPRY2 deficiency alone triggers activation of AKT and ERK, but this is insufficient to drive tumorigenesis.
|
23434594 |
2013 |
Carcinogenesis
|
0.100 |
AlteredExpression
|
phenotype |
BEFREE |
High levels of RUVBL2 promoted carcinogenesis through the heat shock protein 90 (HSP90)-Cell Division Cycle 37 (CDC37), AKT serine/threonine kinase (AKT) and mitogen-activated protein kinase (ERK/MAPK) pathways.
|
31572066 |
2019 |