Abstract:
:The presence of androgen receptor variant 7 (AR-V7) variants becomes a significant hallmark of castration-resistant prostate cancer (CRPC) relapsed from hormonal therapy and is associated with poor survival of CRPC patients because of lacking a ligand-binding domain. Currently, it still lacks an effective agent to target AR-V7 or AR-Vs in general. Here, we showed that a novel class of agents (thailanstatins, TSTs and spliceostatin A analogs) can significantly suppress the expression of AR-V7 mRNA and protein but in a less extent on the full-length AR expression. Mechanistically, TST-D is able to inhibit AR-V7 gene splicing by interfering the interaction between U2AF65 and SAP155 and preventing them from binding to polypyrimidine tract located between the branch point and the 3' splice site. In vivo, TST-D exhibits a potent tumor inhibitory effect on human CRPC xenografts leading to cell apoptosis. The machinery associated with AR gene splicing in CRPC is a potential target for drugs. Based on their potency in the suppression of AR-V7 responsible for the growth/survival of CRPC, TSTs representing a new class of anti-AR-V agents warrant further development into clinical application.
journal_name
Int J Cancerjournal_title
International journal of cancerauthors
Wang B,Lo UG,Wu K,Kapur P,Liu X,Huang J,Chen W,Hernandez E,Santoyo J,Ma SH,Pong RC,He D,Cheng YQ,Hsieh JTdoi
10.1002/ijc.30893subject
Has Abstractpub_date
2017-11-15 00:00:00pages
2121-2130issue
10eissn
0020-7136issn
1097-0215journal_volume
141pub_type
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