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Table 1 Molecular consequences associated with XPO1 inhibition

From: Nucleo-cytoplasmic transport as a therapeutic target of cancer

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]