elevated expression of activated ERK1/2 may play a role in lung metastasis of salivary adenoid cystic carcinoma.

The up-regulation of ERK1/2-dependent thymidylate synthase and thymidine phosphorylase can protect human lung cancer cells from cisplatin-induced cytotoxicity.

Overexpression of MUC1 enhances proangiogenic activity of non-small-cell lung cancer cells through activation of Akt and extracellular signal-regulated kinase pathways.

CAV-1 affected cell growth of lung cancer NCI-H446 cell through the interactions with p-ERK1/2, estrogen receptor and progestin receptor

Data show that p38 MAPK, ERK1/2, and COX-2 activation are mediators for the galectin-1-promoted tumor progression and chemoresistance in lung cancer.

Derlin-1 is overexpressed in non-small cell lung cancer and promotes invasion by EGFR-ERK-mediated up-regulation of MMP-2 and MMP-9.

CAC1 promoted the proliferation of human lung cancer A549 cells with activation of ERK1/2 signaling pathways.

High phosphorylated ERK1 is associated with low response to chemotherapy in nonsmall-cell lung carcinoma.

Therefore, the positivity of p-ERK1/2 expression may serve as a vital biomarker in the development of non-small cell lung cancer

The results of our study suggest that ERK1 and ERK2 have previously unrecognized effects on the Hippo pathway in human non-small cell lung cancer cells

Down-regulation of XRCC1 expression by resveratrol can enhance the chemosensitivity to etoposide in non-small lung cancer cells, via ERK1/2 and AKT signaling .

The aim of this study was to investigate the effect of different ERK1/2 pathway activation, assessed by the expression levels of phosphorylated (p) ERK1/2, on the prognosis of advanced lung adenocarcinoma patients.

Increased SPK1 expression promotes cell growth by activating the ERK1/2 signaling in non-small-cell lung cancer.

NFIA enhances cell radiosensitivity by downregulating p-AKT and p-ERK in non-small cell lung cancer

Differential functions of ERK1 and ERK2 in lung metastasis processes in triple-negative breast cancer.

Results describe the roles of MEK1/ERK and AKT/PKB pathways on the effects of granulocyte macrophage colony-stimulating factor (GM-CSF) and M-CSF on tumor progression of lung cancer.