FAK is up-regulated in NSCLC, and it may have a role in lung cancer progression

Report expression of FAK and PTEN in bronchioloalveolar carcinoma and lung adenocarcinoma.

expression of focal adhesion kinase in small-cell lung carcinoma.

REVIEW: The role of focal adhesion kinase in lung cancer

FAK overexpression is a promising pathological factor to predict aggressive behavior and prognosis in patients with non-small cell lung cancer, particularly in the adenocarcinoma subtype.

our data suggest that the dual inhibition of FAK and EGFR by using plasmid vector-based RNA interference might be a novel therapeutic approach to the treatment of human non-small-cell lung cancer .

High FAK expression is associated with invasion and metastasis of lung squamous cell carcinoma.

Authors propose a model whereby vimentin promotes FAK stabilization through VAV2-mediated Rac1 activation. This model may explain why vimentin expressing metastatic lung cancer cells are more motile and invasive.

MUC5AC interacts with integrin beta4 that mediates phosphorylation of FAK at Y397 leading to lung cancer cell migration.

From our data we conclude that targeting of CXCR4 and FAK may overcome ABCB1 and ABCC1-dependent doxorubicin resistance in non-small cell lung carcinoma cells

results suggest that Kctd20 impacts proliferation and invasion of non-small cell lung cancer through enhancing Fak and Akt phosphorylation

The RNA-editing enzyme ADAR promotes lung adenocarcinoma migration and invasion by stabilizing FAK.

Somatic mutations and Splicing Variants of Focal Adhesion Kinase are associated with Non-Small Cell lung cancer.

Using different human CRC cells lines with differential invasive capacities in an in vivo murine model recapitulating different steps of CRC development from primary tumors to liver and lung metastasis, 3 out of the 8 mRNA variants (FAK0, FAK28 and FAK6) differentially expressed along the CRC process and tumor site. FAK0 and FAK6 splice variant expression was associated with higher aggressiveness and metastatic potential.

Oridonin inhibits the migration and epithelial-to-mesenchymal transition of small cell lung cancer cells by suppressing FAK-ERK1/2 signalling pathway.

Long noncoding RNA Linc00210 promotes non-small cell lung cancer progression via sponging miR-16-5p/PTK2 axis.

intratumoral delivery of Polyethylenimine-complexed plasmids targeting FAK significantly suppressed primary tumor growth as well as metastasis of B16F10 cells into lung and lymph nodes

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

These results demonstrate the critical role of integrin beta(1)-FAK signaling axis in controlling the initial proliferation of micrometastatic cancer cells disseminated in the lungs.

Localized activation of endothelial FAK and E-selectin in the lung vasculature mediates the initial homing of metastatic cancer cells to specific foci in the lungs.

RHOA-FAK is a required signaling axis for the maintenance of kRAS-driven lung adenocarcinomas