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Mechanisms of Nuclear Export in Cancer and Resistance to Chemotherapy

Institute of Cancer Therapeutics, University of Bradford, Bradford, West Yorkshire BD7 1DP, UK
Author to whom correspondence should be addressed.
Academic Editor: Jonas Cicenas
Cancers 2016, 8(3), 35;
Received: 30 January 2016 / Revised: 3 March 2016 / Accepted: 8 March 2016 / Published: 14 March 2016
(This article belongs to the Special Issue Small GTPases in Cancer)
PDF [1663 KB, uploaded 14 March 2016]


Tumour suppressor proteins, such as p53, BRCA1, and ABC, play key roles in preventing the development of a malignant phenotype, but those that function as transcriptional regulators need to enter the nucleus in order to function. The export of proteins between the nucleus and cytoplasm is complex. It occurs through nuclear pores and exported proteins need a nuclear export signal (NES) to bind to nuclear exportin proteins, including CRM1 (Chromosomal Region Maintenance protein 1), and the energy for this process is provided by the RanGTP/RanGDP gradient. Due to the loss of DNA repair and cell cycle checkpoints, drug resistance is a major problem in cancer treatment, and often an initially successful treatment will fail due to the development of resistance. An important mechanism underlying resistance is nuclear export, and a number of strategies that can prevent nuclear export may reverse resistance. Examples include inhibitors of CRM1, antibodies to the nuclear export signal, and alteration of nuclear pore structure. Each of these are considered in this review. View Full-Text
Keywords: Nuclear export; CRM1; Ran; nucleocytoplasmic transport Nuclear export; CRM1; Ran; nucleocytoplasmic transport

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El-Tanani, M.; Dakir, E.-H.; Raynor, B.; Morgan, R. Mechanisms of Nuclear Export in Cancer and Resistance to Chemotherapy. Cancers 2016, 8, 35.

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