Expression of regulatory factor R-spondin family in Wnt signaling pathway in colorectal cancer and its clinical significance
10.11817/j.issn.1672-7347.2017.05.003
- VernacularTitle:Wnt通路新调控因子R-spondin家族在结直肠癌中的表达及其临床意义
- Author:
Heli LIU
;
Yuan ZHOU
;
Fengbo TAN
;
Yinan WANG
;
Haiping PEI
- Keywords:
R-spondinfamily;
β-catenin;
colorectal cancer;
Wnt signaling pathway
- From:
Journal of Central South University(Medical Sciences)
2017;42(5):501-506
- CountryChina
- Language:Chinese
-
Abstract:
Objective:To explore the expression of R-spondin family in colorectal cancer tissues and adjacent tissues,and to evaluate its relationship with clinic-pathological stage.Methods:A total of 64 samples of colorectal cancer tissues and adjacent tissues were collected from the patients,who received radical surgery in Xiangya Hospital,Central South University between January 2014 and August 2014.The mRNA and protein expression levels of R-spondin 1-4 and β-catenin in the colorectal cancer tissues and adjacent tissues were detected by qRT-PCR and immunohistochemistry.The relationship between the expression level of R-spondin 1-4 and the clinic-pathological factors were analyzed to explore the correlation between the expression level of R-spondin 1-4 and β-catenin in colorectal cancer.Results:Compared with the adjacent tissues,the mRNA and protein expression levels of R-spondin 1 were elevated in the colorectal cancer tissues (P＜0.05).The mRNA and protein expression levels of R-spondin 2-4 were increased in the colorectal cancer tissues than those in the normal tissues (P＜0.05),but there was no significant difference between the colorectal cancer tissues and adjacent tissues (P＞0.05).The expression level of R-spondin i was positively correlated with the nuclear expression of β-catenin in the colorectal cancer tissues (r=0.6307,P＜0.05).Conclusion:Compared with the adjacent tissues,the mRNA and protein expression levels of R-spondin 1 are significantly elevated in the colorectal cancer tissues.R-spondin 1 may play a role in promoting carcinogenesis by regulating the activity of β-catenin in the downstream of Wnt signaling pathway.
