Abstract
Canstatin, the non-collagenous domain of collagen type IV α-chains, belongs to a series of collagen-derived angiogenic inhibitors. In this study, the inhibitory effect of recombinant canstatin on tumour growth was investigated using a gastric cancer xenograft model. The volume and weight of tumours in mice treated with canstatin were lower than that in mice treated with PBS. Accordingly, the survival rate of these mice was significantly higher than that of mice bearing tumours treated with PBS. Moreover, valuable insight into the mechanisms mediated by canstatin was obtained.
Highlights
Gastric cancer is the second most common cause of cancer deaths worldwide
We further investigated the anti-angiogenesis and antitumour activity of canstatin and our results showed that it can inhibit the neovascularization of chick chorioallantoic membrane (CAM) and suppress the growth of SGC-7901 in a xenograft model of nude mice through mitochondrial apoptotic pathway
Effect of canstatin on in vivo angiogenesis In order to evaluate the inhibitory effect of canstatin on in vivo angiogenesis, we tested this possibility on vascular endothelial growth factor (VEGF)-induced angiogenesis in the chick CAM
Summary
A total of 989600 new gastric cancer cases and 738000 deaths are estimated to have occurred in 2008 [1]. About 60 % of new cases of gastric cancer occur in eastern Asia [2], especially in China. Some potential molecular targets for therapy in gastric cancer have been reported in previous studies, such as EGFR (epidermal growth factor receptor) [3], VEGF (vascular endothelial growth factor) [4] and RON (recepteur d’origine nantais) [5]. Canstatin inhibits tumour growth in mouse models [10] and is a potent inhibitor of angiogenesis with a distinct antitumour activity [12]
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