Down-regulation of SNX1 predicts poor prognosis and contributes to drug resistance in colorectal cancer

被引:14
|
作者
Bian, Zehua [1 ]
Feng, Yuyang [1 ]
Xue, Yao [1 ]
Hu, Yaling [1 ]
Wang, Qifeng [2 ]
Zhou, Leyuan [1 ]
Liu, Zhihui [1 ]
Zhang, Jiwei [1 ]
Yin, Yuan [1 ]
Gu, Bing [3 ,4 ]
Huang, Zhaohui [1 ]
机构
[1] Jiangnan Univ, Affiliated Hosp, Wuxi Oncol Inst, 200 Huihe Rd, Wuxi 214062, Jiangsu, Peoples R China
[2] Fudan Univ, Shanghai Canc Ctr, Dept Pathol, Shanghai 200032, Peoples R China
[3] Xuzhou Med Coll, Affiliated Hosp, Dept Lab Med, Xuzhou 221002, Jiangsu, Peoples R China
[4] Xuzhou Med Coll, Med Technol Inst, Xuzhou 221002, Jiangsu, Peoples R China
基金
中国国家自然科学基金;
关键词
Sorting nexin 1 (SNX1); Colorectal cancer (CRC); Prognosis; Drug resistance; CELL; PROLIFERATION; TARGETS;
D O I
10.1007/s13277-015-3814-3
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
As a potential tumor suppressor, the detailed clinical application value of sorting nexin 1 (SNX1) has not been elucidated in colorectal cancer (CRC). The aim of the present study was to evaluate the expression of SNX1 in CRC tissues and to determine its correlation with clinicopathologic characteristics and its impact on patient's prognosis. We detected the expression of SNX1 mRNA in 72 CRC patients and SNX1 protein in 237 CRC patients by real-time polymerase chain reaction (RT-PCR) and immunohistochemical staining, respectively. Relationship between the expression of SNX1 and various clinicopathological features in these patients was evaluated. Both the mRNA and protein expression of SNX1 were remarkably decreased in CRC tissues compared with paired non-cancerous tissues, and the down-regulation of SNX1 protein was strongly associated with poor differentiation and poor overall survival (OS) rate of CRC patients. Ectopic SNX1 expression repressed CRC cell growth and promoted tumor sensitivity to most commonly used chemotherapeutic drugs (oxaliplatin and 5-Fluorouracil). In conclusion, overexpression of SNX1 may serve as a new therapeutic strategy for CRC.
引用
收藏
页码:6619 / 6625
页数:7
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