BCL2L1 and prostate carcinoma: In contrast, a study investigating TQ’s activity in models of aggressive prostate cancers (androgen receptor (AR)-independent (C4-2B) and AR naïve (PC-3) prostate cancer cells) showed that in this cellular context, TQ did not increase the activity of caspases, but it significantly upregulated the expression of apoptosis-inducing factor-1, and downregulated the expressions of several Bcl2-related proteins, such as BAG-1, Bcl2, Bcl2A1, Bcl2L1, and BID [21].