Fig. 2. Known interactions between small molecules and the ERSR in glioma.

Several compounds have been investigated for their ERSR inducing apoptotic properties in glioma cells. FLAV treatment results in increased [Ca²⁺]_c. EGCG binds to GRP78 and prevents the formation of antiapoptotic GRP78-caspase 7 complex while also promoting elevated [Ca²⁺]_c. THAP, CELE, DMC, and CUR are potent SERCA inhibitors that lead to reduced [Ca²⁺]_ER. NLG inhibitors (e.g. TUN) prevent N-linked glycosylation of proteins leading to ER retention of unfolded proteins. BFA inhibits protein export from the ER to the Golgi thus promoting ER protein accumulation. BOR, NFZ, ATZ inhibit the proteasome and cause aged and unfolded protein accumulation in the ER.