A permissive role for FAK regulating proliferation and migration provides an essential adhesion checkpoint in cancer progression.
On the plasma membrane, the system can get locally switched on to assemble an adhesion site by passing through checkpoints that enable additional protein interactions in the integrin adhesome.
We propose that at the plasma membrane the system can get locally switched on to self-assemble adhesion sites by passing through checkpoints that induce additional protein interactions in the integrin adhesome.
Poorly differentiated thyroid carcinomas presented molecular signatures related to cell proliferation, poor prognosis, spindle assembly checkpoint and cell adhesion.
The authors suggest that both cell contractility and mechanosensing through focal adhesions are controlled by molecular checkpoints that regulate cell polarization.
Various factors are critical for centrosome clustering, such as cortical actin, the spindle assembly checkpoint (SAC), cell adhesion and polarity regulators, the Ndc80 microtubule-kinetochore attachment complex, augmin complex members, and microtubule motors (e.g., dynein and HSET).
For example, matrix metalloproteinases may act in transformation by inducing apoptosis in anchorage-dependent cells and/or by modifying cell cycle checkpoints through alterations in cell adhesion.
We propose that adhesion receptor polarization is a parenchymal immune checkpoint that allows functional epithelium to hamper leukocyte binding.
As a result, Wee1 may be more than a G2 checkpoint nullifier, since it also affects cell adhesion molecules.
A lack of adhesion signaling in anchorage-dependent cells results in a block at the G1/S checkpoint of the cell cycle [19].
