Modulation of the c-Met/hepatocyte growth factor pathway in small cell lung cancer

HGF stimulation of c-Met-overexpressing H69 small cell lung cancer cells (40 ng/ml, 15 min) resulted in an increase of reactive oxygen species

Using lung adenocarcinoma samples and cell lines derived from lung adenocarcinomas, we demonstrated that the gene copy number for MET in lung adenocarcinoma tissue samples was increased over EGFR, HGF, and PXN and that it correlated with better prognosis

High hgf expression is associated with lung adenocarcinoma.

The cross-talk and balance between HGF/c-Met signal pathways are critical and necessary in the development of new therapies for lung cancer.

low plasma levels are associated with higher response rate to gefitinib in patients with advanced non-small cell lung cancer

HGF-positive serum status had a significant and independent negative effect on progression-free survival among patients with non-squamous non-small cell lung cancer receiving gefitinib or erlotinib and having the wild-type EGFR gene.

suggest that abnormality of the HGF/MET pathway occurs during the course of progression from non-invasive to invasive pulmonary adenocarcinoma

Studies indicate that EGFR signaling in EGFR-mutant lung cancer and hepatocyte growth factor (HGF) ligand-triggered bypass signals (HGF-Met and EGFR ligands-EGFR) must be simultaneously blocked to avoid the resistance.

HGF-induced Met phosphorylation may be an important mechanism of gefitinib resistance in sensitive non-small cell lung cancer

ERK2 but not ERK1 mediates HGF-induced motility in non-small cell lung carcinoma

HGF mediated resistance to alectinib, but not to crizotinib, via the MET signal, that alectinib activated the MET signal in ALK-positive non-small cell lung cancer.

expression of HGFalpha or cMet was closely correlated with VEGFC, lymphatic microvessel density and metastases of lymph nodes, indicating HGFalpha, cMet and VEGFC may perform important and collaborative actions in lymphangiogenesis and lymphatic metastasis of primary non-small-cell lung cancer

HGF and its receptor, cMET, are antagonized in human lung cancer cells treated with YangZheng XiaoJi

miRNA-200a expression was inverse correlation with HGF expression in stromal fibroblasts. High miRNA-200a and low HGF expression in stromal fibroblasts may predict a good prognosis in patients with non-small cell lung cancer.

Data suggest that HGF, IL-20, and IL-22 in the serum and bronchoalveolar lavage fluid (BALF) of non-small cell lung cancer (NSCLC) patients before chemotherapy may be a prognostic of cancer progression.

HGF/c-Met regulates expression of SAE2 and cirRNA CCDC66 to increase epithelial-to-mesenchymal transition and drug resistance of lung adenocarcinoma cells.

Study results revealed a previously uncharacterized role of miRNA200a in regulating tumor malignancy and radiosensitivity of nonsmall cell lung cancer cells by suppressing HGF expression, a key factor in the HGF/cMet pathway.

We found that both protein and gene expression levels of serum cMET, HGF and EGFR were higher in patients with lung cancer. We suggest that protein and gene expression levels of c-MET in patients with lung cancer will lead to targeted therapies as a new biomarker.

Overexpression of hepatocyte growth factor in the airways show increased susceptibility to lung cancer

Mutant CDK4 dramatically increased the number and the growth kinetics of carcinogen-induced primary melanomas in the skin and promoted the growth of spontaneous metastases in lymph nodes and lungs.

NK4 could act on tumor cells to inhibit CT26 adhesion to endothelial cells by reducing FAK phosphorylation, which is regulated by inside-out HGF/c-Met signaling, and thereby suppress hematogenous pulmonary metastasis