Abstract
Cancer cell invasion and metastasis are closely related to intracellular tension. The cell-polarity protein, Par3, is a mechanical transmitter that affects cytoskeletal forces and determines breast cancer aggressiveness. Increased Par3 tension caused by aPKC inactivation is involved in filopodia and lamellipodia formation. Blocking the connection between Par3 and aPKC increases breast cancer aggressiveness both in vitro and in vivo. Meanwhile, aPKC-induced Par3 cytoplasmic translocation results in JAM-A phase separation and microfilament depolymerization, which is associated with increased intracellular protein nanoparticle-induced osmotic pressure. This study demonstrated the effects of aPKC on Par3 tension and osmotic pressure in breast cancer metastasis, and introduced Par3-associated mechanical mechanisms as potential targets for breast cancer treatment.