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

被引：39

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：

070307 [化学生物学]; 071010 [生物化学与分子生物学];

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

页码：861 / 869

页数：9

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