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Comparative proteomic analysis of apoptosis induced by sodium selenite in human acute promyelocytic leukemia NB4 cells
Author(s) -
Dong Hua,
Ying Tianyi,
Li Ting,
Cao Tingming,
Wang Junjun,
Yuan Jing,
Feng Erling,
Han Bingshe,
Hua Fangyuan,
Yang Yang,
Yuan Jiangang,
Wang Hengliang,
Xu Caimin
Publication year - 2006
Publication title -
journal of cellular biochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.028
H-Index - 165
eISSN - 1097-4644
pISSN - 0730-2312
DOI - 10.1002/jcb.20755
Subject(s) - apoptosis , downregulation and upregulation , acute promyelocytic leukemia , microbiology and biotechnology , western blot , signal transduction , c jun , chemistry , kinase , biology , cell culture , transcription factor , biochemistry , gene , retinoic acid , genetics
Selenium (Se) is an essential trace element possessing anticarcinogenic properties. Sodium selenite (Na 2 SeO 3 ) induced apoptosis in human acute promyelocytic leukemia (APL) cell line NB4 with dose and time dependency. In this study, proteomic techniques were used to study the apoptosis of NB4 cells induced by sodium selenite. Twenty‐six downregulated and four upregulated proteins were identified, which exhibited a 1.5‐fold change or greater. The identified proteins included key regulators of signal transduction such as Rho GDP dissociation inhibitor (Rho GDI) alpha and beta members of the MAPK family, and proteins involved in the regulation of c‐fos or c‐myc expression. Importantly, the identified proteins, hnRNP D0B and Rho GDI beta, which were related with the regulation of c‐myc , c‐fos , and c‐jun , were determined by reverse transcription‐polymerase chain reaction (RT‐PCR) to confirm their downregulation in proteomic study. Western blot analysis and RT‐PCR were then performed on three associated proteins: c‐Myc, c‐Fos, and c‐Jun, and their expression were observed to be significantly downregulated. Results showed that certain regulation involved in c‐myc, c‐fos , and c‐jun was present in the apoptosis, and the c‐Myc dependent‐on and Jun N‐terminal kinase (JNK) pathway also play roles. J. Cell. Biochem. © 2006 Wiley‐Liss, Inc.