当前位置： SCI文献检索 > INTERNATIONAL IMMUNOPHARMACOLOGY期刊下所有文献 > Sunitinib malate inhibits intestinal tumor development in male ApcMin/+ mice by down-regulating inflammation-related factors with suppressing β-cateinin/c-Myc pathway and re-balancing Bcl-6 and Caspase-3.

Sunitinib malate inhibits intestinal tumor development in male ApcMin/+ mice by down-regulating inflammation-related factors with suppressing β-cateinin/c-Myc pathway and re-balancing Bcl-6 and Caspase-3.

Abstract：

: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, ApcMin/+ 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 ApcMin/+ 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 β-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-α, IL-1α, IL-1β and IFN-γ 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 ApcMin/+ mice, through inhibiting inflammation-related factors, while suppressing β-cateinin/c-Myc pathway and re-balancing protein levels of Bcl-6 and Caspase-3.

journal_name

Int Immunopharmacol

journal_title

International immunopharmacology

authors

Chen L,Xu P,Xiao Q,Chen L,Li S,Jian JM,Zhong YB

doi

10.1016/j.intimp.2020.107128

subject

Has Abstract

pub_date

2021-01-01 00:00:00

pages

107128

eissn

1567-5769

issn

1878-1705

pii

S1567-5769(20)33595-5

journal_volume

90

pub_type

杂志文章

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