Circulating tumor cells must attach to blood vessel walls to establish metastatic colonies. They extend membrane protrusions — microtentacles — that increase contact area and adhesion. These structures are thin, curved, and dynamic. The expected mechanism: motor proteins actively driving the protrusions outward, as in other cellular extensions like filopodia and lamellipodia where actin polymerization and myosin motors provide the force.
FRAP experiments and simulations show the opposite. The driving force is passive microtubule polymerization — simple addition of tubulin subunits at the growing end. Motor-driven sliding contributes minimally. The microtentacle grows because the polymer grows, not because molecular motors push it.
The curved shape — functionally important because it increases the contact area with vessel walls — emerges from mechanics, not from active steering. Microtubules growing outward while anchored at the centrosome encounter the plasma membrane and buckle. The buckling produces curvature. The curvature produces a hook shape that wraps around vessel features. Form follows from the physics of a confined growing polymer, not from cellular signaling that directs the shape.
The structural point: the cell does less than expected. The functional structure (curved protrusion that enhances adhesion) arises from the simplest possible growth mechanism (polymerization) combined with the simplest possible shaping mechanism (mechanical buckling under confinement). Active machinery is not absent — it organizes the microtubule organizing center — but the protrusion itself is a passive consequence of a growing polymer in a bounded space. Metastasis uses the cheapest available physics.