期刊
CANCER IMMUNOLOGY IMMUNOTHERAPY
卷 66, 期 12, 页码 1597-1608出版社
SPRINGER
DOI: 10.1007/s00262-017-2052-5
关键词
Gastric cancer; IL-6; STAT3; M2 macrophages; Tumor progression
资金
- National Key Research and Development Program of China [2016YFC1302200]
- National Natural Science Foundation of China (NSFC) [81372560]
Interleukin 6 (IL-6) was abundant in the tumor microenvironment and played potential roles in tumor progression. In our study, the expression of IL-6 in tumor tissues from 36 gastric cancer (GC) patients was significantly higher than in non-tumor tissues. Moreover, the number of CD163(+)CD206(+) M2 macrophages that infiltrated in tumor tissues was significantly greater than those infiltrated in non-tumor tissues. The frequencies of M2 macrophages were positively correlated with the IL-6 expression in GC tumors. We also found that IL-6 could induce normal macrophages to differentiate into M2 macrophages with higher IL-10 and TGF-beta expression, and lower IL-12 expression, via activating STAT3 phosphorylation. Accordingly, knocking down STAT3 using small interfering RNA decreased the expression of M2 macrophages-related cytokines (IL-10 and TGF-beta). Furthermore, supernatants from IL-6-induced M2 macrophages promote GC cell proliferation and migration. Moreover, IL-6 production and CD163(+)CD206(+) M2 macrophage infiltration in tumors were associated with disease progression and reduced GC patient survival. In conclusion, our data indicate that IL-6 induces M2 macrophage differentiation (IL-10(high)TGF-beta(IL)-I-high-12 (p35) (low) ) by activating STAT3 phosphorylation, and the IL-6-induced M2 macrophages exert a pro-tumor function by promoting GC cell proliferation and migration.
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