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Signal Transduct Target Ther. 2016 Jul 1;1:16010. doi: 10.1038/sigtrans.2016.10. eCollection 2016.

Inhibiting cancer cell hallmark features through nuclear export inhibition.

Author information

1
State Key Laboratory of Biotherapy and Collaborative Innovation Center of Biotherapy, Sichuan University, Chengdu, China.
2
Department of Pathology, West China Hospital, Sichuan University, Chengdu, China.
3
Department of Internal Medicine, UT Southwestern Medical Center, Dallas, Texas, USA.
4
Department of Molecular Biology, UT Southwestern Medical Center, Dallas, Texas, USA.
5
West China 2nd University Hospital, Sichuan University, Chengdu, China.

Abstract

Treating cancer through inhibition of nuclear export is one of the best examples of basic research translation into clinical application. Nuclear export factor chromosomal region maintenance 1 (CRM1; Xpo1 and exportin-1) controls cellular localization and function of numerous proteins that are critical for the development of many cancer hallmarks. The diverse actions of CRM1 are likely to explain the broad ranging anti-cancer potency of CRM1 inhibitors observed in pre-clinical studies and/or clinical trials (phase I-III) on both advanced-stage solid and hematological tumors. In this review, we compare and contrast the mechanisms of action of different CRM1 inhibitors, and discuss the potential benefit of unexplored non-covalent CRM1 inhibitors. This emerging field has uncovered that nuclear export inhibition is well poised as an attractive target towards low-toxicity broad-spectrum potent anti-cancer therapy.

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