analysis of reciprocal regulation of c-Src and STAT3 in non-small cell lung cancer

Increased expression of PGE2 in the lung tumor microenvironment may initiate a mitogenic signaling cascade composed of EP4, betaArrestin1, and c-Src which mediates cancer cell migration.

Data show that the signaling events that accompany the CDCP1 tyrosine phosphorylation observed in cell lines and lung tumors may explain how the CDCP1/SFK complex regulates motility and adhesion.

Confluence of cultured lung cancer cells dramatically increases STAT3 activation independent of SRC action.

ARHGEF5/Src can be considered as a prognostic biomarker and a therapeutic target for patients with resected non-small cell lung cancer .

Src-mediated ERK reactivation may play a role in a novel gefitinib resistance mechanism in non small cell lung cancer.

We conclude that AFB1 may upregulate IRS2 and stimulate lung cancer cell migration through Src

Data suggest that Src kinases inhibitors may act with different mechanisms in non-small cell lung cancer (NSCLC) depending on EGF receptor (EGFR)/Ras protein (Ras) mutational profile.

Data show that src kinases (SRC) and mitogen-activated protein kinase kinase 1 (MEK) co-inhibition by saracatinib and PD0325901 respectively can be broadly effective in tumor growth control of a wide panel of non-small cell lung cancer (NSCLC) cell lines.

Dasatinib, a c-Src inhibitor, dephosphorylated caspase-8 to facilitate necroptosis, rather than apoptosis, in paclitaxel-treated p-Casp8-expressing lung adenocarcinoma cells.

Findings indicate the importance of Src-Stat3 signaling cascade in gallic acid (GA)-mediated tumor-suppression activity and a therapeutic insight of GA for acquired resistance to EGF receptor tyrosine kinase inhibitors in lung cancer.

Overexpression of SRC is associated with lung cancer.

Our data suggest that targeting Src signaling may be an effective approach to the treatment of ALK-non-small cell lung cancer (NSCLC) with acquired resistance to ALK inhibitors.

High Src family kinase expression is associated with vinorelbine resistance in lung cancer.

X-ray irradiation induced the aggregation of lipid rafts and the clustering of c-Met and c-Src to lipid rafts through both lipid raft-dependent and lipid raft-independent mechanisms. The lipid raft-dependent activation of c-Met and its downstream pathways played an important role in the development of radiation resistance in non-small cell lung cancer cells mediated by c-Met.

High SRC expression is associated with lung adenocarcinoma.

Src-mediated vascular permeability is essential for tumor metastasis to the lung but is not required to support angiogenesis or the growth of tumor cells in vivo.