JUN and central nervous system cancer: On the other hand, the treatment with both HCA and C21:5n-3 compounds trigger ER stress and the UPR pathway, as shown by the increase of c-Jun phosphorylation and BiP induction, and they enhance autophagic flux by increasing the conversion of LC3B-I to LC3B-II and SQSTM1/p62 levels [22], as already observed in glioma cells [11].