Reverse correlation of Jab1 and Smad4 in PANC-1 cells involved in the pathogenesis of pancreatic cancer

被引:0
作者
Li, Jun [1 ]
Gu, Zhuoyu [2 ]
Li, Siyuan [2 ]
Xiao, Zhiwei [2 ]
Sun, Kan [1 ]
机构
[1] Shihezi Univ, Sch Med, Affiliated Hosp 1, Dept Endocrinol, Shihezi 832002, Peoples R China
[2] Shihezi Univ, Coll Med, Xinjiang Endem & Ethn Dis, Key Lab,Minist Educ, Shihezi 832002, Peoples R China
关键词
Jab1; Smad4; TGF-beta; pancreatic cancer; DEGRADATION; JAB1/CSN5; DPC4; UBIQUITINATION; STATISTICS; P27(KIP1); STABILITY; PATHWAY; CHINA; GENE;
D O I
暂无
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
Objective: Steps in the genetic basis of pancreatic cancer (PC) have been recently identified, however, Studies focusing on the relationship between Jab1 and Smad4 in PC are rarely reported. This study was performed to examine the expression patterns and association of Jab1 and Smad4 in PC cells for gaining a further understanding of PC pathogenesis. Methods: Human pancreatic cancer cell line PANC-1 cells were infected with retrovirus vector containing GFP, HA-Jab1, siGFP, and siJab1 respectively. The expression of Jab1 and Smad4 in PANC-1 cells was analyzed by Western blot and immunocytochemistry. Subsequently, the effect of overexpression of Jab1 on cell proliferation inhibition mediated by TGF-beta was examined with MTT colorimetry. Results: The expression of Smad4 in PANC-1 cells was inhibited after the overexpression of Jab1. Inversely, the expression of Smad4 was increased after the down-regulation of Jab1 silenced by SiRNA. Smad4 expression in PANC-1 cells was negatively correlated with Jab1 expression. In addition, the cell proliferation inhibitory effect induced by TGF-beta in PANC-1 cells was attenuated after the overexpression of Jab1. Conclusions: The reverse correlation of Jab1 and Smad4 in PANC-1 cells may be involved in the Pathogenesis of PC. Jab1 can cause degradation of Smad4 via TGF-beta signal pathway, consequently contributing to the proliferation of PC cells.
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页数:7
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