PRL-3, Phosphatase of regenerating liver 3, is part of the PRL family of phosphatases responsible for cellular proliferation and growth of various cancers. Western Blot analyses shows that PRL-3, among other proteins, decreases in expression when Triple Negative Breast Cancer, TNBC, cells are treated with Selinexor. Selinexor is marketed to be selective inhibitor of nuclear export or a SINE drug and is currently in clinical trials for treating various cancers. Past work has shown that selinexor kills HCC1143, and BT549 TNBC cell lines 24-48 hours after treatment. It has been suggested in other studies that gene knock-outs of PRL-3 leads to the unviability of cancer lines. Molecular docks using AutoDock Vina shows potential binding of selinexor into the active site of PRL-3 with moderate binding affinity. This computational work suggests binding <i>in vitro</i> which could be responsible for the death of TNBC cells, likely through direct inhibition of PRL-3.<br/>

Computational study of PRL-3 in complex with the selective inhibitor of nuclear export selinexor

2019 Spring National Meeting

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