Table 1.

Molecular consequences associated with XPO1 inhibition

Target (nuclear accumulation)	Biological effects	References
Cyclin D1	Protein degradation, reduction of cell proliferation and increased apoptosis	[17],[31]
p21	Reduction of cell proliferation	[17]
p27	Reduction of cell proliferation	[18],[34]
p53	Restoration of nuclear p53 and p53-mediated response to stress	[16],[30],[33],[59]
FOXO proteins	Activates the transcription of genes that promote cell cycle arrest, apoptosis and down-modulate Wnt/β-catenin signals	[30],[34]-[39]
IκB	Attenuates constitutively activated NF-κB and causes apoptosis in cancer cells	[40]-[42]
BRCA1	Resistance versus PARP inhibitors	[43]-[45]
Survivin	Increased apoptosis	[46]-[51]
Fbw7	Degrades nuclear Notch-1 leading to decreased tumor promoting markers such as C-Myc, Cyclin-D1, Hes1 and VEGF.	[52]
Topo IIα	Sensitization to Topoisomerase II poisons	[53]
Nucleophosmin	Once within the nucleus it could, in principle drive Bax translocation.	[54]-[56]
FAS activation	Activation of intrinsic apoptosis pathway	[57],[58],[60],[61]