| First Author | Chen L | Year | 2021 |
| Journal | Int Immunopharmacol | Volume | 90 |
| Pages | 107128 | PubMed ID | 33191180 |
| Mgi Jnum | J:314332 | Mgi Id | MGI:6822043 |
| Doi | 10.1016/j.intimp.2020.107128 | Citation | Chen L, et al. (2021) Sunitinib malate inhibits intestinal tumor development in male Apc(Min/+) mice by down-regulating inflammation-related factors with suppressing beta-cateinin/c-Myc pathway and re-balancing Bcl-6 and Caspase-3. Int Immunopharmacol 90:107128 |
| abstractText | Sunitinib is a tyrosine kinase inhibitor for many tumors. Inflammation is one of the most important factors in the development of intestinal tumors. Many inflammation-related factors are regulated by tyrosine kinase receptors. It is reasonable to hypothesize that sunitinib can regulate the development of intestinal tumors by regulating the expression and/or activity of inflammation-related factors. Here, Apc(Min/+) male mouse model was used to investigate the effect and mechanism of sunitinib malate against intestinal cancer. Results show that compared to vehicle, after sunitinib malate treatment, overall survival of Apc(Min/+) mice was lengthened up to 25 days, with a gain of body weight, reduction of spleen/body weight index, and RBC, WBC and HGC regulated to normal levels of wild type mice, and a number of polyps no less than 1 mm significantly reduced. Meanwhile, in the intestines, the nuclear beta-Catenin protein and c-Myc mRNA were both down-regulated, and Bcl-6 was significantly reduced with Caspase-3 up regulated. Furthermore, inflammation-related factors including IL-6, TNF-alpha, IL-1alpha, IL-1beta and IFN-gamma were down-regulated at mRNA levels in the intestines. These results suggest that sunitinib malate can significantly improve the survival status and inhibit intestinal tumor development in male Apc(Min/+) mice, through inhibiting inflammation-related factors, while suppressing beta-cateinin/c-Myc pathway and re-balancing protein levels of Bcl-6 and Caspase-3. |
