The CM exposure influences prostate cell progression through increasing cytoplasmic accumulation of β-catenin, which subsequently leads increased migration.

<p>Further, inflammation-mediated Akt activity and subsequent β-catenin transactivation can be deregulated by androgen responsive factor NKX3.1, stabilizing the p-β-catenin^(S33) pool, eventually influencing the maintenance of the intact β-catenin/E-cadherin association at the plasma membrane.