Title : Concurrent blockade of NF-κB and Akt pathways potentiates cisplatin's antitumor activity in vivo.

Pub. Date : 2012 Nov

PMID : 22760211






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1 Concurrent blockade of NF-kappaB and Akt pathways potentiates cisplatin"s antitumor activity in vivo. Cisplatin thymoma viral proto-oncogene 1 Mus musculus
2 Our previous study has demonstrated that NF-kappaB and Akt cooperatively blunt cytotoxicity induced by cisplatin or etopside in different types of cancer cells in vitro, indicating that the concurrent blocking of these pathways may effectively improve the anticancer efficacy of anticancer therapeutics. Cisplatin thymoma viral proto-oncogene 1 Mus musculus
3 In this study, we further investigated the effect of concurrent blockade of NF-kappaB and Akt on the anticancer activity of cisplatin in vivo in a xenograft tumor model. Cisplatin thymoma viral proto-oncogene 1 Mus musculus
4 The resultant cells with concurrent NF-kappaB and Akt blockade were significantly more sensitive to cisplatin-induced cell death in vitro. Cisplatin thymoma viral proto-oncogene 1 Mus musculus
5 Consistently, tumors derived from cells with the concurrent blockade of NF-kappaB and Akt were much more sensitive to cisplatin compared with those derived from cells with individual blockage of NF-kappaB or Akt in a nude mouse xenograft tumor model. Cisplatin thymoma viral proto-oncogene 1 Mus musculus
6 These results show for the first time that the concurrent blockage of the NF-kappaB and Akt pathways cooperatively potentiates the antitumor activity of cisplatin in vivo, indicating that this strategy may be potentially useful for clinical anticancer therapy. Cisplatin thymoma viral proto-oncogene 1 Mus musculus