Promising SINEs for embargoing nuclear-cytoplasmic export as an anticancer strategy

Cancer Discov. 2014 May;4(5):527-37. doi: 10.1158/2159-8290.CD-13-1005. Epub 2014 Apr 17.


In cancer cells, the nuclear-cytoplasmic transport machinery is frequently disrupted, resulting in mislocalization and loss of function for many key regulatory proteins. In this review, the mechanisms by which tumor cells co-opt the nuclear transport machinery to facilitate carcinogenesis, cell survival, drug resistance, and tumor progression will be elucidated, with a particular focus on the role of the nuclear-cytoplasmic export protein. The recent development of a new generation of selective inhibitors of nuclear export (XPO1 antagonists) and how these novel anticancer drugs may bring us closer to the implementation of this therapeutic strategy in the clinic will be discussed.

Publication types

  • Review

MeSH terms

  • Active Transport, Cell Nucleus / drug effects*
  • Antineoplastic Agents / therapeutic use*
  • Cell Survival / drug effects
  • Clinical Trials as Topic
  • Drug Resistance, Neoplasm
  • Gene Expression Regulation, Neoplastic
  • Humans
  • Karyopherins / antagonists & inhibitors*
  • Neoplasms / drug therapy*
  • Neoplasms / genetics
  • Receptors, Cytoplasmic and Nuclear / antagonists & inhibitors*
  • Short Interspersed Nucleotide Elements*


  • Antineoplastic Agents
  • Karyopherins
  • Receptors, Cytoplasmic and Nuclear
  • exportin 1 protein