title: Reverse correlation of Jab1 and Smad4 in PANC-1 cells involved in the pathogenesis of pancreatic cancer.
abstract: 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-β 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-β 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-β signal pathway, consequently contributing to the proliferation of PC cells.
authors.affiliation: Department of Endocrinology, First Affiliated Hospital, Medical School of Shihezi University Shihezi 832002, China.
authors.forename: Jun
authors.initials: J
authors.lastname: Li
authors.affiliation: Key Laboratory of Ministry of Education, Xinjiang Endemic and Ethnic Diseases, Medical College of Shihezi University Shihezi 832002, China.
authors.forename: Zhuoyu
authors.initials: Z
authors.lastname: Gu
authors.affiliation: Key Laboratory of Ministry of Education, Xinjiang Endemic and Ethnic Diseases, Medical College of Shihezi University Shihezi 832002, China.
authors.forename: Siyuan
authors.initials: S
authors.lastname: Li
authors.affiliation: Key Laboratory of Ministry of Education, Xinjiang Endemic and Ethnic Diseases, Medical College of Shihezi University Shihezi 832002, China.
authors.forename: Zhiwei
authors.initials: Z
authors.lastname: Xiao
authors.affiliation: Department of Endocrinology, First Affiliated Hospital, Medical School of Shihezi University Shihezi 832002, China.
authors.forename: Kan
authors.initials: K
authors.lastname: Sun
mesh_terms: D000075686:COP9 Signalosome Complex; D045744:Cell Line, Tumor; D049109:Cell Proliferation / Q000187:drug effects / Q000235:genetics; D006801:Humans; D047908:Intracellular Signaling Peptides and Proteins / Q000235:genetics / Q000378:metabolism*; D010190:Pancreatic Neoplasms / Q000235:genetics / Q000378:metabolism* / Q000473:pathology; D010447:Peptide Hydrolases / Q000235:genetics / Q000378:metabolism*; D015398:Signal Transduction / Q000187:drug effects / Q000235:genetics; D051901:Smad4 Protein / Q000235:genetics / Q000378:metabolism*; D016212:Transforming Growth Factor beta / Q000494:pharmacology
chemical_list: D047908:Intracellular Signaling Peptides and Proteins; D051901:Smad4 Protein; D016212:Transforming Growth Factor beta; D010447:Peptide Hydrolases; C501488:COPS5 protein, human; D000075686:COP9 Signalosome Complex
keywords: Jab1; Smad4; TGF-β; pancreatic cancer