Title : Nuclear Export of Ubiquitinated Proteins Determines the Sensitivity of Colorectal Cancer to Proteasome Inhibitor.

Pub. Date : 2017 Apr

PMID : 27903750






4 Functional Relationships(s)
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1 Inhibition of CRM1, the nuclear export carrier protein, hampered protein export and synergistically enhanced the cytotoxic action of bortezomib on colon cancer cells containing wild-type p53, which underwent G2-M cell-cycle block and apoptosis. Bortezomib tumor protein p53 Homo sapiens
2 Moreover, knockdown of p53 significantly reduced the synergistic cytotoxic action of bortezomib and KPT330 on p53+/+ HCT116 cells. Bortezomib tumor protein p53 Homo sapiens
3 Moreover, knockdown of p53 significantly reduced the synergistic cytotoxic action of bortezomib and KPT330 on p53+/+ HCT116 cells. Bortezomib tumor protein p53 Homo sapiens
4 These results indicate that nuclear p53 is a major mediator in the synergistic antitumor effect of bortezomib and KPT330, and provides a rationale for the use of proteasome inhibitor together with nuclear export blocker in the treatment of colorectal cancer. Bortezomib tumor protein p53 Homo sapiens