# Lung Cancers: Parenchymal Biochemistry and Mechanics

## TL;DR

Lung cancer tissues show muscle-like contractile properties, driven by specific proteins and signaling pathways.

## Contribution

Discovery of contractile properties in lung cancer parenchyma and their relation to non-muscle myosin and β-catenin/WNT pathway activation.

## Key findings

- Lung cancer tissues exhibit contractile properties similar to muscles but with ultraslow kinetics.
- Contractility is driven by non-muscle myosin type II A and II B.
- Activation of the β-catenin/WNT pathway correlates with high non-muscle myosin levels in lung cancers.

## 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.