MOESM2 of Increased neutrophil extracellular traps promote metastasis potential of hepatocellular carcinoma via provoking tumorous inflammatory response
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Additional file 2: Figure S1. NETs formation was enhanced in HCC associated neutrophils. Figure S2. Depositions of NETs was correlated with metastasis burden in HCC. Figure S3. NETs in HCC bearing mice. Figure S4. Evidence of NETs formation in TCGA and The Human Protein Atlas database. Figure S5. HCC enhanced the NETs formation capacity of normal neutrophils. Figure S6. NETs formation was enhanced in HCC-driven inflammatory condition in mice. Figure S7. Effect of DNase 1 and neutrophil depletion on LPS-induced NETs in mice. Figure S8. NETs trap optimized adhesion of HCC, and further promoted metastasis potential by raising invasion capacity with minimal cytotoxicity. Figure S9. Effect of DNase 1 on inflammatory mediators expression in NETs-stimulated HCC cells. Figure S10. Correlation analysis of infiltrated neutrophils and COX2 or other inflammatory mediator genes in TIMER database. Figure S11. Pearson correlation analysis of PADI4/MPO and COX2 or other inflammatory mediator genes in TCGA database. Figure S12. Effects of inhibiting IL-1 and TNF-α on NETs-aroused metastasis potential. Figure S13. HCQ impaired the enhanced metastasis potential triggered by NETs. Figure S14. Targeting NETs abrogated tumorous inflammatory response.
补充材料2：图S1。肝细胞癌（Hepatocellular Carcinoma, HCC）相关中性粒细胞中中性粒细胞胞外陷阱（Neutrophil Extracellular Traps, NETs）的形成增强。 图S2。肝细胞癌中NETs沉积与肿瘤转移负荷相关。 图S3。荷肝细胞癌小鼠体内的NETs。 图S4。癌症基因组图谱（The Cancer Genome Atlas, TCGA）与人类蛋白质图谱（The Human Protein Atlas, HPA）数据库中NETs形成的相关证据。 图S5。肝细胞癌可增强正常中性粒细胞的NETs形成能力。 图S6。小鼠肝细胞癌驱动的炎症环境中NETs形成增强。 图S7。脱氧核糖核酸酶1（Deoxyribonuclease 1, DNase 1）与中性粒细胞耗竭对小鼠脂多糖（Lipopolysaccharide, LPS）诱导的NETs的影响。 图S8。NETs可优化肝细胞癌的黏附能力，并通过提升侵袭能力在极轻微细胞毒性的前提下进一步增强其转移潜能。 图S9。脱氧核糖核酸酶1对经NETs刺激的肝细胞癌细胞中炎症介质表达的影响。 图S10。肿瘤免疫评估资源（Tumor Immune Estimation Resource, TIMER）数据库中浸润性中性粒细胞与环氧合酶2（Cyclooxygenase 2, COX2）及其他炎症介质基因的相关性分析。 图S11。TCGA数据库中肽酰精氨酸脱亚胺酶4（Peptidylarginine Deiminase 4, PADI4）/髓过氧化物酶（Myeloperoxidase, MPO）与COX2及其他炎症介质基因的皮尔逊相关性分析。 图S12。抑制白细胞介素1（Interleukin-1, IL-1）与肿瘤坏死因子α（Tumor Necrosis Factor-α, TNF-α）对NETs诱导的转移潜能的影响。 图S13。羟氯喹（Hydroxychloroquine, HCQ）可削弱NETs触发的转移潜能增强效应。 图S14。靶向NETs可消除肿瘤性炎症反应。
