JUN and infection: GSK3β signaling promoted by infection, activated NF-κB-mediated expression of proinflammatory molecules and inhibited the activity of β-catenin, Nrf2, CREB, STAT1/3, and cJun-AP1, except in MCF7 and MDA-MB-231 stimulated with LPS (Tables 1, S1, 2 and Figure 2).