Primary malignant neoplasm
|
0.100 |
Biomarker
|
group |
BEFREE |
ERK1/2 activation is fundamental for the development and progression of cancer.
|
31126017 |
2019 |
Primary malignant neoplasm
|
0.100 |
Biomarker
|
group |
BEFREE |
Acid ceramidase (AC) is a promising target protein in the development of multi-targeted anticancer drugs as its inhibition can simultaneously inhibit angiogenesis via the Akt and ERK 1/2 pathway and limit cancer growth through ceramide-induced apoptosis.
|
30661200 |
2019 |
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 |
AlteredExpression
|
group |
BEFREE |
Airway normal and cancer epithelial cells (16HBE and A549) were exposed to cigarette smoke extracts (CSE) or with/without agomiR-21, and then it was assessed: a) miR-21 expression; b) signal transducer and activator of transcription 3 (STAT3) nuclear protein expression and ERK1/2 activation; c) IL-8 gene expression and protein release.
|
31054160 |
2019 |
Primary malignant neoplasm
|
0.100 |
Biomarker
|
group |
BEFREE |
Along with our previous report that ERK1 promotes HDAC6 activity, we propose that HDAC6 and ERK1 may form a positive feed-forward loop, which might play a role in cancer.
|
29259132 |
2018 |
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 |
AlteredExpression
|
group |
BEFREE |
Conversely, exposure of cancer cells to arsenic showed a lower level of production of Ras and p‑ERK as well as higher level of p‑ERK1 and p‑ERK2 as compared to control group.
|
29328451 |
2018 |
Primary malignant neoplasm
|
0.100 |
Biomarker
|
group |
BEFREE |
Cyclooxygenase-2 (COX-2) and extracellular signal-regulated kinase 1/2 (ERK1/2) may serve as potential targets in various types of cancer; however, the roles of these proteins in gallbladder carcinoma (GBC) have not been reported previously.
|
28521485 |
2017 |
Primary malignant neoplasm
|
0.100 |
Biomarker
|
group |
BEFREE |
Effects of long non-coding RNA (lncRNA) cancer susceptibility candidate 2c (CASC2c) on proliferation, metastasis and drug resistance of non-small cell lung cancer (NSCLC) cells through ERK1/2 and β-catenin signaling pathways.
|
31300295 |
2019 |
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 |
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 |
Finally, <b>P-A</b> inhibited the ERK1/2 and AKT signaling in the above two cancer cell lines.
|
28420180 |
2017 |
Primary malignant neoplasm
|
0.100 |
AlteredExpression
|
group |
BEFREE |
Finally, TEM8-Fc, a recombinant fusion protein comprising the extracellular domain of human TEM8 linked to the Fc portion of human IgG1, efficiently abrogated the interaction between uPA and TEM8, blocked uPA-induced migration of HepG2 cells in vitro and inhibited the growth and metastasis of human MCF-7 xenografts in vivo. uPA, TEM8 and EGFR overexpression and ERK1/2 phosphorylation were found co-located on frozen cancer tissue sections.
|
30241478 |
2018 |
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 |
GeneticVariation
|
group |
BEFREE |
GABBR2 was significantly downregulated, along with the reduction of S6, p-p70 S6, and p-ERK1/2, demonstrating that GABBR2 may play an important role in EGFR signaling through the ERK1/2 pathway.<b>Conclusions:</b> We demonstrated that <i>GABBR2</i> gene might be a novel potential epigenetic treatment target with induction erlotinib treatment for stage IIIa (N2) <i>EGFR</i> 19 deletion lung adenocarcinoma.<i>Clin Cancer Res; 23(17); 5003-14.©2017 AACR</i>.
|
28490462 |
2017 |
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 |
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 |
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 |
In a previous study, we showed that actin disruption delays mitotic entry at G2/M by sustained activation of extracellular signal-related kinase 1/2 (ERK1/2) in primary cells but not in transformed cancer cell lines.
|
29754473 |
2018 |
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 |
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 |
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 |
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 |
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 the present study, two kisspeptin phosphinic peptides were designed and synthesized, and their ability to induce phosphorylation of ERK1/2 through kisspeptin receptor and their inhibition on MMP-2 and MMP-9 whose activity correlates with cancer metastasis were assessed.
|
29614094 |
2018 |