癌症研究
生物
基因沉默
基因敲除
STAT蛋白
血管生成
上皮-间质转换
白细胞介素8
癌症
细胞生长
车站3
转移
癌变
细胞培养
信号转导
免疫学
细胞因子
细胞生物学
基因
生物化学
遗传学
作者
Ying Qiao,Chunhua Zhang,Aoya Li,D Wang,Zhen Luo,Ping Yü,Bohao Zhou,S Liu,Hongyu Li,Dongli Yue,Zijian Zhang,X Chen,Zhibo Shen,Jingyao Lian,Y Li,S Wang,F Li,Lan Huang,Lihui Wang,B Zhang,Jane Yu,Zhihai Qin,Yi Zhang
出处
期刊:Oncogene
[Springer Nature]
日期:2017-10-23
卷期号:37 (7): 873-883
被引量:137
摘要
Various factors and cellular components in the tumor microenvironment are key drivers associated with drug resistance in many cancers. Here, we analyzed the factors and molecular mechanisms involved in chemoresistance in patients with esophageal squamous cell carcinoma (ESCC). We found that interleukin 6 (IL6) derived mainly from cancer-associated fibroblasts played the most important role in chemoresistance by upregulating C-X-C motif chemokine receptor 7 (CXCR7) expression through signal transducer and activator of transcription 3/nuclear factor-κB pathway. CXCR7 knockdown resulted in the inhibition of IL6-induced proliferation and chemoresistance. In addition, CXCR7 silencing significantly decreased gene expression associated with stemness, chemoresistance and epithelial–mesenchymal transition and suppressed the proliferation ability of ESCC cells in three-dimensional culture systems and angiogenesis assay. In clinical samples, ESCC patients with high expression of CXCR7 and IL6 presented a significantly worse overall survival and progression-free survival upon receiving cisplatin after operation. These results suggest that the IL6–CXCR7 axis may provide a promising target for the treatment of ESCC.
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