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PF-04691502 Triggers Cell Cycle Arrest, Apoptosis and Inhibits the Angiogenesis in Hepatocellular Carcinoma Cells

PF-04691502 Triggers Cell Cycle Arrest, Apoptosis and Inhibits the Angiogenesis in Hepatocellular Carcinoma Cells

Feng-Ze Wang, Peng-Jiao, Na-Na Yang, Chuang-Yuan, Ya-Li Zhao, Qiang-Qiang Liu, Hong-Rong Fei, Ji-Guo Zhang

Toxicol Lett. 2013 Jul 4;220(2):150-6.

PMID: 23639247

Abstract:

Hepatocellular carcinoma (HCC) is a major cause of morbidity and mortality in the world. The aim of the present study is to determine the antitumor effect of PF-04691502, a potent inhibitor of PI3K and mTOR kinases, on the apoptosis and angiogenesis of the hepatoma cancer cells. Our results indicate that treatment of cancer cells with PF-04691502 reduces cell viability and inhibits cell growth in a dose-dependent manner. PF-04691502 triggers apoptosis via a mitochondrial pathway, accompanied by activation of caspase-3, caspase-9, and poly(ADP-ribose) polymerase (PARP). Pre-treatment of hepatoma cells with the caspase-3 inhibitor (z-DEVD-fmk) blocks the PF-04691502-induced death of these cells. In addition, growth factors-induced tube formation and the migration of HUVECs are markedly inhibited by PF-04691502 treatment. The mechanisms of anti-angiogenesis of PF-04691502 are associated with inhibiting the expression of VEGF and HIF-1α. Based on the overall results, we suggest that PF-04691502 reduces hepatocellular carcinoma cell viability, induces cell apoptosis, and inhibits cell growth and tumor angiogenesis, implicating its potential therapeutic value in the treatment of HCC.

Chemicals Related in the Paper:

Catalog Number	Product Name	Structure	CAS Number	Price
AP1013101364	PF-04691502		1013101-36-4	Price

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