Silencing of CXCR2 and CXCR7 protects against esophageal cancer

被引:1
|
作者
Wu, Kai [1 ]
Cui, Lingling [2 ]
Yang, Yang [1 ]
Zhao, Jia [1 ]
Zhu, Dengyan [1 ]
Liu, Donglei [1 ]
Zhang, Chunyang [1 ]
Qi, Yu [1 ]
Li, Xiangnan [1 ]
Li, Weihao [1 ]
Zhao, Song [1 ]
机构
[1] Zhengzhou Univ, Affiliated Hosp 1, Dept Thorac Surg, 1 Jianshe East Rd, Zhengzhou 450000, Peoples R China
[2] Zhengzhou Univ, Coll Publ Hlth, Zhengzhou 450000, Henan, Peoples R China
来源
关键词
Esophageal cancer; CXCR2; CXCR7; SiRNA; clinicopathological features; progression; CHEMOKINE RECEPTOR CXCR7; CELLS IN-VITRO; TUMOR-GROWTH; CLINICAL-SIGNIFICANCE; EXPRESSION; PROLIFERATION; ADENOCARCINOMA; ANGIOGENESIS; SURVIVAL; VIVO;
D O I
暂无
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
This study was aimed to investigate the functional roles of cytokine receptor (CXCR) CXCR2 and CXCR7 in esophageal cancer (EC). Specific small interfering RNAs (siRNA) against CXCR2 and CXCR7 were transfected into EC cell lines TE-1, EC9706, and EC109 cells. Expression of CXCR2 and CXCR7 was validated, along with cell viability, chemotaxis, apoptosis rate, and ERK1/2 pathways associated protein after transfection. Moreover, EC9706 cells treated with or without CXCR2/7 siRNA were injected into athymic nude mice. Tumor volumes were measured. Besides, immunohistochemical (IHC) staining was performed to investigate the expression of CXCR2/7 in adjacent normal tissues and tumor tissues from esophageal squamous cell carcinoma (ESCC) patients. Also, the associations between CXCR2/7 expression and clinicopathological features and progression were explored. The mRNA levels of CXCRmotaxis, and increased apoptotic rate. Cells invasion was significantly reduced by 2 and CXCR7 were significantly reduced after transfection. Silencing of CXCR2 and CXCR7 statistically decreased cell viability and chesilencing of CXCR2, however, no significance was found in silencing of CXCR7. The protein levels of pERK1/2 were significantly decreased by silencing of CXCR2 and CXCR7. Besides, silencing of CXCR2 and CXCR7 significantly reduced tumor growth in vivo, and associated with clinicopathological features and progression. Silencing of CXCR2 and CXCR7 protects against EC by inhibiting cell growth and chemotaxis, and inducing apoptosis though ERK1/2 pathways. Silencing of CXCR2 and CXCR7 has potentially therapeutic target for EC.
引用
收藏
页码:3398 / 3408
页数:11
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