The
integrin receptor
protein talin plays vital roles in intracellular chemical and mechanical activities, and it is implicated in the high invasion and poor prognosis of
non-small cell lung cancer (NSCLC). To better understand the mechanism underlying the function of
talin in NSCLC invasion and
metastasis, a few newly designed tension probe based on Förster resonance energy transfer was used for real-time observation of tension changes in A549 cells. High NSCLC cell aggressiveness was found to be accompanied with inward
talin and outward
glial fibrillary acidic protein (GFAP) tensions, which are closely associated with microfilament (MF) force and intracellular osmotic potential. The increased osmotic pressure resulted from the production of intracellular
protein nanoparticles and the related ion influx. Furthermore,
integrin activation was found to adjust the
talin and GFAP tensions. Disruption of the interaction between
talin and MFs blocked the mechanical source of
talin, reducing both
talin tension and osmotic pressure and thus inhibiting NSCLC cell invasion and migration. Consequently, our study demonstrates that
talin is involved in NSCLC invasion and migration via its inward tension and that the
integrin pathway is correlated closely with
protein-nanoparticle-induced outward osmotic pressure.