Abstract
Parenchyma of pulmonary cancers acquires contractile properties that resemble those of muscles but presents some particularities. These non-muscle contractile tissues could be stimulated either electrically or chemically (KCl). They present the Frank-Starling mechanism, the Hill hyperbolic tension-velocity relationship, and the tridimensional time-independent tension-velocity-length relationship. Relaxation could be obtained by the inhibition of crossbridge molecular motors or by a decrease in the intracellular calcium concentration. They differ from muscles in that their kinetics are ultraslow as evidenced by their low shortening velocity and myosin ATPase activity. Contractility is generated by non-muscle myosin type II A and II B. The activation of the β-catenin/WNT pathway is accompanied by the high level of the non-muscle myosin observed in lung cancers.