We are analyzing https://link.springer.com/article/10.1007/s00262-017-2052-5.

Title:
Interleukin 6 induces M2 macrophage differentiation by STAT3 activation that correlates with gastric cancer progression | Cancer Immunology, Immunotherapy
Description:
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-β 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-β). 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-10highTGF-βhighIL-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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pubmed, article, google, scholar, cas, macrophages, cancer, macrophage, central, stat, cell, activation, gastric, progression, expression, immunol, tumor, interleukin, polarization, tumorassociated, poor, prognosis, induces, cells, signaling, nat, wang, privacy, cookies, content, research, zhao, access, tumour, blood, sica, china, data, publish, search, immunology, differentiation, august, duan, yuan, zhuang, tissues, patients, human, breast,

Topics {✒️}

yong-sheng teng & yuan zhuang month download article/chapter pei-wu yu yong-liang zhao cd163+cd206+ m2 macrophages m2 macrophages-related cytokines il-10hightgf-βhighil-12 lowp35 angioimmunoblastic t-cell lymphoma national key research article cancer immunology yong-sheng teng induces m2 polarization m2-polarized macrophages 6/il-6 receptor axis gastric cancer progression full article pdf leukemia inhibitory factor fang-yuan mao privacy choices/manage cookies m2 macrophage expression colorectal cancer cells yuan zhuang advanced thyroid cancer chong-yu su cell cycle arrest m-1/m-2 macrophages primary effusion lymphoma article fu anti-cancer therapy vivo predicts effectors anti-inflammatory response epithelial–mesenchymal transition induce normal macrophages alternatively activated macrophages activating stat3 phosphorylation jak2/stat3 pathway lower il-12 expression bmc cancer 15 european economic area yi-ping lv tris-buffered saline cigarette smoke extract ricarte-filho jcm military medical university excellent technical assistance ethics declarations conflict article log conditions privacy policy gastric adenocarcinoma patients m2 tumour

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         description: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-β 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-β). 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-10highTGF-βhighIL-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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