ERK1/2 is activated in non-small-cell lung cancer and associated with advanced tumours

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.

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

PRL-3 up-regulates pERK and Rho expression and activity in lung cancer

mitogen-activated protein kinase phosphatase-1 has a role in non-small cell lung carcinomas

Activated p38 MAPK is associated with lung adenocarcinoma.

Data show that ALK inhibitor-induced apoptosis is mediated both by BIM upregulation resulting from inhibition of ERK signaling as well as by survivin downregulation resulting from inhibition of STAT3 signaling in EML4-ALK-positive lung cancer cells.

Upregulation of ERK2/ERK1 signaling pathway was found to be responsible for cisplatin resistance in non-small-cell lung cancer cells.

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.

activation of RAF1-MEK1-ERK/AKT axis may determine the resistance of non-small cell lung cancer cell lines bearing wild type EGFR to erlotinib

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

These results identify Erk2 as the key downstream signal transducer between Met activation and EGFR ligand upregulation in squamous cell carcinoma cell lines derived from tongue, larynx and lung.

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 .

Phloretin is able to inhibit NSCLC A549 cell growth by inducing apoptosis through P38 MAPK and JNK1/2 pathways, and therefore may prove to be an adjuvant to the treatment of non-small cell lung cancer

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.

High p38 MAPK expression is associated with cisplatin resistance in lung cancer.

urthermore, MAPK signaling may control the expression of PD-L1 and several genes related to enhanced cell motility. Our findings suggest that MAPK, along with STAT3, is important for determining PD-L1 expression, which could be useful for targeted therapies against lung cancers.

p38MAPK-hyaluronan-dependent reprogramming of the tumor microenvironment plays a critical role in driving lung tumorigenesis.

it was observed cellular accumulation of ROS upon compound treatment and an activation of the stress-kinase p38 MAPK route that, when inhibited, reverted the cytotoxic effect of the tambjamine analogues. Finally, a significant therapeutic effect of these compounds was observed in subcutaneous and orthotopic lung cancer mice models

RNF25 plays an essential role in gefitinib resistance of Non-small cell lung cancer by mediating cross-talk between NF-kappaB and ERK pathways.

These results illustrated that oleuropein-induced apoptosis via mitochondrial apoptotic cascade was activated by the p38 MAPK signaling pathway in H1299 cells. Thus, oleuropein as a natural compound and therapeutic drug has potential application value in the treatment of lung cancer.

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

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

mitogen-activated protein kinase phosphatase-1 as a potential pharmacological target in non-small cell lung carcinomas