CacyBP/SIP enhances multidrug resistance of pancreatic cancer cells by regulation of P-gp and Bcl-2

被引：24
|
作者：
Chen, Xiong [1 ]
Zheng, Peichan [2 ]
Xue, Zengfu [3 ]
Li, Jie [1 ]
Wang, Wenwu [1 ]
Chen, Xi [1 ]
Xie, Fangwei [1 ]
Yu, Zongyang [1 ]
Ouyang, Xuenong [1 ]
机构：
[1] Nanjing Mil Command, Dept Med Oncol, Fuzhou Gen Hosp, Fuzhou, Fujian, Peoples R China
[2] Fujian Med Univ, Sch Basic Med Sci, Dept Anat, Fuzhou, Fujian, Peoples R China
[3] Xiamen Univ, Affiliated Hosp 1, Dept Digest Dis, Xiamen, Fujian, Peoples R China
来源：
APOPTOSIS | 2013年 / 18卷 / 07期
基金：
中国国家自然科学基金;
关键词：
CacyBP/SIP; Multidrug resistance; Apoptosis; Pancreatic cancer; BINDING-PROTEIN; EXPRESSION; TUMORIGENICITY; TARGET;
D O I：
10.1007/s10495-013-0831-9
中图分类号：
Q5 [生物化学]; Q7 [分子生物学];
学科分类号：
071010 ; 081704 ;
摘要：
Our former report indicates that calcyclin-binding protein or Siah-1-interacting protein (CacyBP/SIP) is over-expressed in the SGC7901/ADR cell line. However, the potential role of CacyBP/SIP in the development of multidrug resistance (MDR) of pancreatic cancer is still uncertain. In this paper, we investigated the role of CacyBP/SIP in MDR of pancreatic cancer cells and its possible underlying mechanisms, and found that CacyBP/SIP was over-expressed in the Gemcitabine induced MDR pancreatic cancer cell PC-3/Gem compared with its parental cell PC-3. Up-regulation of CacyBP/SIP expression could enhance resistance of chemotherapy drugs on PC-3 cells and inhibit Adriamycin-induced apoptosis accompanied by decreased accumulation of intracellular Adriamycin. Furthermore, CacyBP/SIP could significantly up-regulate the expression of P-gp, Bcl-2, and the transcription of the MDR1 gene. In addition, the decrease of CacyBP/SIP expression using RNA interference or P-gp inhibitor could partially reverse CacyBP/SIP-mediated MDR. In brief, our study demonstrated that CacyBP/SIP could enhance the MDR phenotype of pancreatic cancer cells by increasing the expression of P-gp and Bcl-2, thus inhibiting apoptosis of pancreatic cancer cell.
引用
收藏
页码：861 / 869
页数：9
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