Capn4 is induced by and required for Epstein-Barr virus latent membrane protein 1 promotion of nasopharyngeal carcinoma metastasis through ERK/AP-1 signaling.
Moreover, SATB1 expression and anoikis resistance were mainly regulated by HBV-encoded viral protein HBx through the activation of ERK and p38 MAPK signaling pathways to promote metastasis of liver cancer.
Furthermore, the inhibition of ERK activation instead of Akt activation was found to participate in erlotinib-mediated metastasis resistance, including anoikis, inhibition of EMT, migration, and invasion.
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.
In addition, DCLK1 overexpression induced the ERK MAPK pathway, which resultantly enhanced the expression of MT1-MMP that is also involved in cancer metastasis.
In this current study, VCP979, which is a novel p38 MAPK inhibitor with safety and efficacy in inhibiting the activity of serine threonine protein kinase, effectively suppressed orthotopic pancreatic cancer growth and metastasis.
Ribosomal S6 Kinase 2 (RSK2) is a downstream target of ERK1/2 in MAPK/ERK pathway and inhibition of RSK2 suppresses the tumorigenesis and metastasis of neoplasm.
Eventually, it was proved that COL4A5 promoted peritoneal metastasis by activating Wnt signaling pathway, whereas the upregulation of integrin family genes mediated by FAK-AKT/ERK/STAT3 signaling pathway activation is involved in peritoneal metastasis promotion function of EMCN.
Furthermore, TBMS1 combined with TBHQ (an ERK activator) dramatically suppressed TBMS1‑induced apoptosis and stimulated TBMS1‑reduced migration and invasion in NCI‑H1299 cells, suggesting that TBMS1 inhibits the ERK signaling pathway and represses the growth and metastasis of NCI‑H1299 cells.
Taken together, these findings provide new evidence that mitogen-activated protein kinase/extracellular signal regulated kinase (MAPK/ERK) signaling pathway plays an important role in promoting invasion and metastasis in HepG2 cells through p-ERK, and MAPK/ERK signaling pathway may be a therapeutic target for tumor.
These compounds downregulate the extracellular signal-regulated kinase/mitogen-activated protein kinase (ERK/MAPK) pathway to inhibit cell growth, proliferation, and metastasis through the matrix metalloproteinases (MMPs) MMP2 and MMP9 in A549 cells.
Supervillin promotes epithelial-mesenchymal transition and metastasis of hepatocellular carcinoma in hypoxia via activation of the RhoA/ROCK-ERK/p38 pathway.
CSCs-exosomes also decreased apoptosis (marked by downregulation of <i>Bax</i> and <i>p53</i> and upregulation of <i>Bcl2</i>, and increased immunostaining of PCNA), increased angiogenetic activity (revealed by upregulation of <i>VEGF</i>), enhanced metastasis and invasiveness (indicated by upregulation of P13K and ERK proteins and their downstream target <i>MMP9</i> and downregulation of <i>TIMP1</i>), and induced epithelial mesenchymal transition (marked by increased serum and hepatic level of TGF<i>β</i>1 mRNA and protein).