Fig. 11

DDX5 (also called p68 in early studies) plays important roles in multiple treatment resistant mechanisms: This includes, but may not be limited to, promoting DNA repair and R-loop resolution during DNA replication and gene transcription (this review); promoting immune suppression (this review); controlling cancer metabolism (this review); promoting oncogene expression (e.g., survivin, Mcl1, XIAP, cIAP2, MdmX, ERCC6, c-Myc, mutant Kras (mKras), etc., which can be indirectly inhibited by FL118 [46, 133, 139, 140]); controlling various types of RNA metabolism (e.g., pre-RNA, long and short/small non-coding RNA) and ribosome biogenesis [141]; promoting virus infection and replication (this review); and negatively influences microbiota (this review). On the other hand, while FL118 targets DDX5, FL118 could also bypass many other treatment resistant mechanisms (e.g., overexpression (OE) of ABCG2/BCRP [142, 143] and/or OE of P-gp/MDR-1 [142]; null/mutated p53 (n/mut p53) [140]; cancer stem cell (CSC)-induced treatment resistance [144], etc.)