Intestinal mucosal tissue and polyps isolated from Mlkl<sup>-/-</sup> mice exhibited increased ERK activation and elevated expression of genes associated with inflammation and cancer.
Major contributions to reducing prostate cancer cell numbers included low E<sub>2</sub> concentrations producing sustained ERK phospho-activation correlated with generation of reactive oxygen species causing cancer cell death, and phospho-activation of cyclin D1 triggering its rapid degradation by interrupting cell cycle progression.
These differentially abundant proteins were related to nuclear factor κB (NF-κB) and p38 mitogen-activated protein (MAP) kinase pathways and were involved in cellular compromise, inflammatory response, and cancer.
Two isoforms of extracellular regulated kinase (ERK), namely ERK-1 and ERK-2, are associated with several cellular processes, the aberration of which leads to cancer.
We demonstrate that IKKα signaling promotes increased cell malignancy of NSCLC cells as well as lung tumor progression and metastasis in either subcellular localization, through activation of common protumoral proteins, such as Erk, p38 and mTor.
Flow cytometry and western blot analysis demonstrated the fact that anticancer activity was closely related with cancer cell apoptosis and the blockade of the phosphorylation of c-Met and its downstream signaling ERK and Akt.
In this review, we summarize our current understanding of the roles of the ERK and JNK pathways in controlling the Warburg effect in cancer and discuss their implication in controlling this metabolic reprogramming in physiological processes and opportunities for targeting their downstream effectors for therapeutic purposes.
The findings of the present study indicated that Sirt7 affects the malignancy of glioma cells mainly in promoting glioma proliferation and invasion through ERK and STAT3 signaling.
The expression of p-ERK and Mps1 in CRC with BRAF<sup>V600E</sup> was significantly higher compared with in CRC with BRAF<sup>WT</sup> (P<0.05), and their expression is associated with cancer classification, degree of differentiation and lymph node transfusion (P<0.05).
In mucoepidermoid carcinomas, pERK1/ERK2 expression was associated with low-grade malignancy, positive nuclear survivin, and better disease-specific survival.
Knockdown of BMPR1a of breast cancer cells suppresses their production of RANKL via p38 pathway and inhibits cancer-induced osteoclastogenesis, which indicates that BMPR1a might be a possible target in breast cancer-induced osteolytic metastasis.
In this study, two cancer cell lines were used to evaluate the cytotoxicity and apoptotic effect of Sg-AgNP along with the determination of the role of the Caspase-3 / p38 MAPK pathways.
In this issue of <i>Science Signaling</i>, Yuan <i>et al.</i> report that MEK1 homodimerization is necessary for signal transduction through the RAF-ERK pathway and that cancer-related MEK1 mutations confer enhanced dimerization and resistance to MEK inhibitors.