Title : Blocking CDK1/PDK1/β-Catenin signaling by CDK1 inhibitor RO3306 increased the efficacy of sorafenib treatment by targeting cancer stem cells in a preclinical model of hepatocellular carcinoma.

Pub. Date : 2018

PMID : 30083256






6 Functional Relationships(s)
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1 Blocking CDK1/PDK1/beta-Catenin signaling by CDK1 inhibitor RO3306 increased the efficacy of sorafenib treatment by targeting cancer stem cells in a preclinical model of hepatocellular carcinoma. Sorafenib cyclin dependent kinase 1 Homo sapiens
2 Blocking CDK1/PDK1/beta-Catenin signaling by CDK1 inhibitor RO3306 increased the efficacy of sorafenib treatment by targeting cancer stem cells in a preclinical model of hepatocellular carcinoma. Sorafenib cyclin dependent kinase 1 Homo sapiens
3 Mechanistic and functional studies silencing CDK1 with shRNA and RO3306 combined with sorafenib abolished oncogenic function via downregulating CDK1, with downstream PDK1 and beta-Catenin inactivation. Sorafenib cyclin dependent kinase 1 Homo sapiens
4 Mechanistic and functional studies silencing CDK1 with shRNA and RO3306 combined with sorafenib abolished oncogenic function via downregulating CDK1, with downstream PDK1 and beta-Catenin inactivation. Sorafenib cyclin dependent kinase 1 Homo sapiens
5 Conclusion: Anti-CDK1 treatment can boost sorafenib antitumor responses in PDX tumor models, providing a rational combined treatment to increase sorafenib efficacy in the clinic. Sorafenib cyclin dependent kinase 1 Homo sapiens
6 Conclusion: Anti-CDK1 treatment can boost sorafenib antitumor responses in PDX tumor models, providing a rational combined treatment to increase sorafenib efficacy in the clinic. Sorafenib cyclin dependent kinase 1 Homo sapiens