|
Primary malignant neoplasm
|
0.100 |
PosttranslationalModification
|
group |
BEFREE |
We have previously reported in a series of papers that a Kunitz-type protease inhibitor, bikunin, suppresses up-regulation of urokinase-type plasminogen activator (uPA) and its specific receptor (uPAR) expression, phosphorylation of ERK1/2 and cancer cell invasion in vitro and peritoneal disseminated metastasis in vivo.
|
15168733 |
2004 |
|
Primary malignant neoplasm
|
0.100 |
AlteredExpression
|
group |
BEFREE |
Treatment of these cancer cell lines with the proteasome inhibitor ZLLF-CHO increased MKP-1 but not MKP-2 expression and decreased ERK1/2 phosphorylation.
|
15243131 |
2004 |
|
Primary malignant neoplasm
|
0.100 |
Biomarker
|
group |
BEFREE |
Growth inhibition of cancer cells is dependent on ROS and ERK1/2 induction as indicated by a significantly reduced PDTC-associated growth inhibition by the free radical scavenger N-acetyl-L-cysteine (NAC) or the MEK/ERK1/2 inhibitor (PD98059).
|
16904205 |
2006 |
|
Primary malignant neoplasm
|
0.100 |
Biomarker
|
group |
BEFREE |
These results reveal that PEA-15 regulates cancer cell invasion via its ability to bind ERK1/2 and indicate that nuclear entry of ERK1/2 is important in tumor behavior.
|
17308092 |
2007 |
|
Primary malignant neoplasm
|
0.100 |
Biomarker
|
group |
BEFREE |
In summary CRPV early protein 2 activates the expression of MMP-9 in-trans through AP-1 and ERK1 and may contribute to cancer development and progression via this mechanism within the animal model.
|
18951930 |
2009 |
|
Primary malignant neoplasm
|
0.100 |
AlteredExpression
|
group |
BEFREE |
In addition, levels of alpha-catenin S641 phosphorylation correlate with levels of ERK1/2 activity in human glioblastoma specimens and with grades of glioma malignancy.
|
19941816 |
2009 |
|
Primary malignant neoplasm
|
0.100 |
Biomarker
|
group |
BEFREE |
Exposure of two human non-small lung cancer (NSCLC) cell lines (A549 and H1975) to curcumin could suppress MMC-induced MKK1/2-ERK1/2 signal activation and Rad51 protein expression.
|
21810436 |
2011 |
|
Primary malignant neoplasm
|
0.100 |
Biomarker
|
group |
BEFREE |
Selumetinib is an inhibitor of ERK1/2 signalling and has been given safely to human subjects in clinical trials for cancer.
|
22068161 |
2012 |
|
Primary malignant neoplasm
|
0.100 |
AlteredExpression
|
group |
BEFREE |
In contrast to the healthy controls, TLR4 expression and the ERK1/2 signaling pathway appear to play only minor roles in APRIL induction in the cells of patients with cancer.
|
23010686 |
2013 |
|
Primary malignant neoplasm
|
0.100 |
Biomarker
|
group |
BEFREE |
Activation of the ERK1/2 pathway is a major determinant of diverse cellular processes and cancer development and is responsible for the transcription of several important miRNAs.
|
23012423 |
2012 |
|
Primary malignant neoplasm
|
0.100 |
Biomarker
|
group |
BEFREE |
Epidermal growth factor (EGF) and interleukin (IL)-1β synergistically promote ERK1/2-mediated invasive breast ductal cancer cell migration and invasion.
|
23083134 |
2012 |
|
Primary malignant neoplasm
|
0.100 |
GeneticVariation
|
group |
BEFREE |
Furthermore, recently identified ERK1/2-inducing mutations in MEK1 and MEK2 (MEK1/2) MAPK genes in melanoma confer resistance to emerging therapeutic MEK inhibitors, underscoring the challenges facing direct kinase inhibition in cancer.
|
23603816 |
2013 |
|
Primary malignant neoplasm
|
0.100 |
Biomarker
|
group |
BEFREE |
Interestingly, whereas macrophage-mediated cancer cell c-Src and ERK1/2 phosphorylation occurred downstream EGFR activation, Akt phosphorylation seems to be a parallel event, taking place in an EGFR-independent manner.
|
23644655 |
2014 |
|
Primary malignant neoplasm
|
0.100 |
AlteredExpression
|
group |
BEFREE |
We demonstrated that PtAcD (1) is more cytotoxic in cancer than in normal breast cells; (2) activated NAD(P)H oxidase, leading to PKC-ζ and PKC-α translocations; (3) activated antiapoptotic pathways based on the PKC-α, ERK1/2 and Akt kinases; (4) activated PKC-ζ and, only in cancer cell PKC-δ, responsible for the sustained phosphorylation of p38 and JNK1/2, kinases both of which are involved in the mitochondrial apoptotic process.
|
24030148 |
2013 |
|
Primary malignant neoplasm
|
0.100 |
Biomarker
|
group |
BEFREE |
Taken together, we propose that a combination of Trail and an inhibitor of ERK 1/2 activities could potentially enhance of Trail's effectiveness as an anti-cancer agent in ERK 1/2 hyperactive cancer cells.
|
24342355 |
2014 |
|
Primary malignant neoplasm
|
0.100 |
Biomarker
|
group |
BEFREE |
Their anticancer mechanisms of action, after binding to specific receptors on cancer cells, include targeting the Rat sarcoma-bound guanosine triphosphate (RAS) (95% inhibition)-mitogen activated protein kinase kinase 1/2 (MEK-1/2) (98% inhibition)-extracellular signal-related kinases 1/2 (ERK-1/2) (96% inhibition) cascade in cancer cells.They also inhibit MAPK9, i.e. c-JUN-N-terminal kinase 2.
|
24692673 |
2014 |
|
Primary malignant neoplasm
|
0.100 |
GeneticVariation
|
group |
BEFREE |
BRAF(V600E) phosphorylates and activates the MEK1 and MEK2 kinases, which in turn phosphorylate and activate the ERK1 and ERK2 kinases, stimulating the mitogen-activated protein kinase (MAPK) pathway to promote cancer.
|
24717435 |
2014 |
|
Primary malignant neoplasm
|
0.100 |
Biomarker
|
group |
BEFREE |
Signals from IL-17B-IL-17RB activated CCL20/CXCL1/IL-8/TFF1 chemokine expressions via the ERK1/2 pathway to promote cancer cell invasion, macrophage and endothelial cell recruitment at primary sites, and cancer cell survival at distant organs.
|
25732306 |
2015 |
|
Primary malignant neoplasm
|
0.100 |
Biomarker
|
group |
BEFREE |
Spontaneous response to extrinsic Wnt signals induces signaling networks comprising ERK1/2 and epithelial-mesenchymal transition that subsequently confer cancer stemness traits to susceptible cells.
|
25769727 |
2015 |
|
Primary malignant neoplasm
|
0.100 |
Biomarker
|
group |
BEFREE |
Our data provide evidence of heterogeneity in ovarian serous carcinoma and identify APC, MAPK3, BAG3 and S100A10 as potential biomarkers of poor chemotherapy response and/or poor outcome in this cancer.
|
26232338 |
2015 |
|
Primary malignant neoplasm
|
0.100 |
AlteredExpression
|
group |
BEFREE |
The present study aimed to investigate the effects of the TLR7 agonist, gardiquimod, on ERK1/2 signaling pathway, and on the expression of genes involved in the pathogenesis of cancer, including phosphatase and tensin homolog deleted on chromosome 10 (PTEN), p53, type Ⅲ interferon (IFN-λ1), vascular endothelial growth factor (VEGF), matrix metalloproteinase 9 (MMP-9) and tissue inhibitor of metalloproteinase 1 (TIMP-1).
|
26718740 |
2016 |
|
Primary malignant neoplasm
|
0.100 |
Biomarker
|
group |
BEFREE |
In experimental models YKL-40 supports tumor initiation through binding to RAGE, and is able to induce cancer cell proliferation via ERK1/2-MAPK pathway.
|
26733160 |
2016 |
|
Primary malignant neoplasm
|
0.100 |
Biomarker
|
group |
BEFREE |
However, our evidence shows that when ERK1/2 are activated and the Raf-1 gene is not mutated, Raf-1 is not hyperphosphorylated in these cells, indicating that ERK1/2 are not responsible for the Raf-1 hyperphosphorylation in these cancer cell lines.
|
27841865 |
2017 |
|
Primary malignant neoplasm
|
0.100 |
Biomarker
|
group |
BEFREE |
Hopefully, the increase of knowledge based on these methods will open more opportunities for the identification of new therapeutic targets for diseases where the ERK1/2 cascade is dysregulated, such as cancer, neurodegenerative diseases, and diabetes.
|
27924567 |
2017 |
|
Primary malignant neoplasm
|
0.100 |
Biomarker
|
group |
BEFREE |
In signaling cascades, RSK2 is regulated under the control of extracellular signal-regulated kinase 1 (ERK1) and 2 (ERK2) activities and is positioned upstream of transcription and epigenetic factors involved in cell proliferation, cell transformation and cancer development, as well as some kinases that modulate cell cycle progression.
|
28013489 |
2017 |