Interleukin-1α induces immunosuppression by mesenchymal stem cells in promoting the growth of prostate cancer cells
10.3760/cma.j.issn.1000-6702.2014.04.015
- VernacularTitle:白细胞介素-1α诱导间充质干细胞产生免疫抑制作用促进前列腺癌细胞生长的研究
- Author:
Jiwen CHENG
;
Qinggui MENG
;
Chengzhong MA
;
Qingyun ZHANG
;
Honghua ZHOU
;
Xianzhong BAI
- Publication Type:Journal Article
- Keywords:
Mesenchymal stem cells;
Prostate cancer cells;
Interleukin-1α;
Immunosuppression
- From:
Chinese Journal of Urology
2014;35(4):297-300
- CountryChina
- Language:Chinese
-
Abstract:
Objective To explore the preliminary mechanism of mesenchymal stem cells (MSCs) in promoting prostate cancer proliferation in tumor inflammatory microenvironment.Methods From April 2013 to October 2013,MSCs pretreated with inflammatory cytokine IL-1α (MSCs (IL-1α)) and its culture supernatants mixed with RM-1 cells,which origined from C57BL/6 mice,were subcutaneously administered in the armpit area of C57BL/6 or BALB/c mice to establish homologous or heterologous transplant animal mode and to detect the tumor growth.Meanwhile the influence of MSCs on the proliferation of spleen cells was detected in vitro.Results In homologous transplant model,the relative tumor weight of prostate cancer cells prtreated with MSCs and MSCs (IL-1α) and their culture supernatant were (3.4 ± 0.2),(3.3 ±0.2),(4.9±0.5),and (5.2±0.6) g.The results were statistically significant (P＜0.05) compared with the control group (2.4±0.2) g.In heterologous model,the ratio of tumor formation of the pretreated groups were 50％,50％,80％ and 80％,respectively,compared with the control group of 0％.The results were statistically significant (P＜0.05).In proliferation experiments of spleen cells,the number of spleen cell pretreated with IL-1α were significantly lower than that in control group and unpretreated group (P ＜ 0.05).Conclusions MSCs pretreated with IL-1α could effectively promote the growth of prostate cancer cell in vivo.The reason may be due to inflammatory cytokines induce immune suppression of MSCs and then lead to immune escape of cancer cells.
