Expression of granulocyte colony-stimulating factor receptor in colitis-associated colonic carcinogenesis
10.3760/cma.j.issn.0253-3766.2018.09.003
- VernacularTitle: 粒细胞集落刺激因子受体及其阳性免疫细胞在结直肠癌发生发展中的表达变化
- Author:
Wei WANG
1
;
Wei YUAN
2
;
Xundong WEI
3
;
Jun QI
1
;
Jie MA
3
Author Information
1. Department of Clinical Laboratory, National Cancer Center/National Clinical Research Center for Cancer/Cancer Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing 100021, China
2. State Key Laboratory of Molecular Oncology, National Cancer Center/National Clinical Research Center for Cancer/Cancer Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing 100021, China
3. Department of Biotherapy, Beijing Hospital, National Center of Gerontology, Beijing 100730, China
- Publication Type:Journal Article
- Keywords:
Colorectal neoplasms;
Granulocyte-colony stimulating factor receptor;
Macrophage;
Immune cell subpopulation;
Inflammatory bowel disease
- From:
Chinese Journal of Oncology
2018;40(9):653-658
- CountryChina
- Language:Chinese
-
Abstract:
Objective:To investigate the expression of granulocyte-colony stimulating factor receptor (G-CSFR) in a mouse model of colitis-associated cancer (CAC), and the roles of G-CSFR positive immune cells in the development of CAC.
Methods:The C57BL/6 mouse model of CAC was established by azoxymethane and dextran sulphate sodium. Three different stages in the development of CAC, including inflammation (AD1), mild dysplasia (AD2) and adenocarcinoma (AD3) were simulated. Colon tissue was digested into single cell suspension and the expressions of G-CSF and G-CSFR were analyzed by real-time PCR and fluorescence activated cell sorter (FACS). The expressions of G-CSFR on T cell, macrophage and neutrophil were analyzed by FACS.
Results:The establishment of mouse model can effectively simulate the disease progression of CAC. The results of real-time PCR detection showed that the expression level of G-CSF mRNA in AD1, AD2 and AD3 groups were 1.2, 7.3 and 18.0-fold changes of the control group, respectively. The differences between AD2, AD3 and control groups were statistically significant (P<0.05). G-CSFR mRNA levels in AD1, AD2 and AD3 groups were 1.5, 2.2 and 4.5-fold changes of the control group, respectively. The difference between AD3 and control groups was statistically significant (P<0.05). FACS showed that the percentages of CD45+ G-CSFR+ cells in colorectal tissues of the control group, AD1, AD2 and AD3 groups were (21.84±1.77)%, (41.48±4.15)%, (44.84±8.54)% and (57.76±1.95)%, respectively.The percentages of CD45+ G-CSFR+ cells in AD2 and AD3 groups were significantly higher than that of control group (P<0.05). The percentages of CD45+ G-CSFR+ macrophage in the colorectal tissues of the control group, AD1, AD2 and AD3 groups were (21.54±5.88)%, (47.14±5.25)%, (42.49±7.80)% and (29.25±8.24)%, respectively. The percentages of CD45+ G-CSFR+ T cells in these groups were (30.04±6.87)%, (29.65±8.08)%, (33.75±7.37)% and (33.32±9.85)%, respectively. The percentages of CD45+ G-CSFR+ granulocyte were (2.39±2.10)%, (4.05±1.56)%, (3.62±2.67)% and (2.26±0.85)%, respectively (P<0.05). The percentages of G-CSFR+ macrophage and G-CSFR+ T cells were significantly higher than that of G-CSFR+ granulocyte (P<0.05). The differences between AD1 and control group, AD2 and control group, AD1 and AD2 group, AD2 and AD3 group were statistically significant (P<0.05).
Conclusions:The expression of G-CSFR is significantly up-regulated in the development of CAC. The enrichment of G-CSFR+ macrophages in the colon tissue suggests G-CSFR+ macrophages participate in the development of CAC.
