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Effects of Disulfiram on Apoptosis in Panc-1 Human Pancreatic Cancer Cell Line



Nikbakht Dastjerdi M1 ; Babazadeh Z1 ; Rabbani M2 ; Gharagozloo M3 ; Esmaeili A4 ; Narimani M5
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Authors Affiliations
  1. 1. Department of Anatomical Sciences and Molecular Biology, Medical School, Isfahan University of Medical Sciences, Isfahan, Iran
  2. 2. Department of Pharmacology, School of Pharmacy and Pharmaceutical Sciences, Isfahan University of Medical Sciences, Isfahan, Iran
  3. 3. Department of Immunology, Medical School, Isfahan University of Medical Sciences, Isfahan, Iran
  4. 4. Cell, Molecular and Developmental Biology Division, Faculty of Sciences, University of Isfahan, Isfahan, Iran
  5. 5. School of Medicine, Kurdistan University of Medical Science, Kurdistan, Iran

Source: Research in Pharmaceutical Sciences Published:2014

Abstract

Pancreatic carcinoma is currently considered as a rapidly progressive and fatal disease, and is typically diagnosed late in its natural course. It is characterized by a poor diagnosis and lack of response to conventional therapy. Recent studies have suggested that disulfiram (DSF), a member of the dithiocarbamate family, may have antitumor activity. This study aimed to evaluate the in vitro effect of DSF on apoptosis in human pancreatic cancerous cell line (PANC-1). PANC-1 cells were cultured and treated with DSF at doses of 5, 10, 13 μM for 24 h and apoptosis was measured. Methylation specific PCR (MS-PCR) and real-time quantitative PCR were carried out to detect the methylation pattern and to estimate the mRNA expression levels of RASSF1A, p21 and Bax. MS-PCR analysis demonstrated that no unmethylated band was apeared in PANC-1 cell line after DSF treatments. The real-time quantitative PCR results showed no significant mRNA expression for RASSF1A (p>0.05); whereas p21 and Bax expression were significantly (p<0.01) enhanced after treatment with DSF. The results of the current study indicated that DSF can induce appoptosis in PANC-1 through p21 and Bax pathway but not through RASSF1A.
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