Capn4 is induced by and required for Epstein-Barr virus latent membrane protein 1 promotion of nasopharyngeal carcinoma metastasis through ERK/AP-1 signaling.
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, 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.
In addition, DCLK1 overexpression induced the ERK MAPK pathway, which resultantly enhanced the expression of MT1-MMP that is also involved in cancer metastasis.
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.
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.
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.
A total of 69 candidate proteins were identified in the protein microarray experiment, including the most highly enriched protein Shoc2, which is a scaffold protein that modulates cell motility and metastasis through the ERK pathway.
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.
Collectively, our results indicated that FGF18 played an important role in the growth and metastasis of breast cancer via the ERK/c‑Myc signaling pathway and EMT, indicating that FGF18 may be a potential molecular treatment target for breast cancer.
Supervillin promotes epithelial-mesenchymal transition and metastasis of hepatocellular carcinoma in hypoxia via activation of the RhoA/ROCK-ERK/p38 pathway.
Meanwhile, key molecules of PI3K/Akt and MAPK/ERK pathways were downregulated, which might be involved in the inhibition against proliferation and metastasis of A375 cells by Oxyfadichalcone C. In addition, combination of Oxyfadichalcone C with Vemurafenib at a ratio of IC50 <sub>Oxyfadichalcone C</sub>: 5 × IC<sub>50 Vemurafenib</sub> exhibited synergistic anti-proliferative effect on A375 cells.
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.
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).
Together, we have identified an association of genetic variants and genes in the RTK/ERK pathway with prostate cancer aggressiveness, and highlighted the potential importance of CCND2 in prostate cancer susceptibility and tumor progression to metastasis.