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A P53 target gene, PIG11, contributes to chemosensitivity of cells to arsenic trioxide
Author(s) -
Liang Xiao-Qiu,
Cao En-Hua,
Zhang Yan,
Qin Jing-Fen
Publication year - 2004
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/j.febslet.2004.05.057
Subject(s) - arsenic trioxide , transfection , green fluorescent protein , apoptosis , chemistry , microbiology and biotechnology , intracellular , cancer research , gene , biology , biochemistry
The tumor suppressor p53 regulates the expression of various genes that promote apoptosis. PIG11 (P53‐induced gene 11), also referred to as TP53I11 (tumor protein p53 inducible protein 11), is a direct p53 target gene. Recent data demonstrated that PIG11 was up‐regulated markedly in arsenic trioxide induced apoptosis by DDRT‐PCR, suggesting a new class of p53 target genes that sensitize cells to the effects of chemotherapeutic agents. In this study, through the construction of a recombinant GFP‐PIG11 expression vector and transfection of HEK293 cells with GFP or GFP‐PIG11, the role of PIG11 in apoptosis was analyzed. Results demonstrated that the percentage (11.38%) of apoptotic cells with GFP‐PIG11 transfection was higher than that (7.28%) of with only GFP transfection ( P <0.05). At 24 h after 1 μM of arsenic trioxide treatment, apoptotic cells exhibited a significant increase in the expression of GFP‐PIG11 (36.67% ± 2.78), in contrast, 10.50% ± 2.03 only GFP and 5.25% ± 0.96 vehicle control ( P <0.01). In addition, we showed that intracellular content of reactive oxygen species (ROS) was 9.66 ± 0.52 in GFP‐PIG11 transfection, higher than 5.21 ± 0.08 in GFP only and 5.99 ± 0.45 in vehicle control ( P <0.01). The above results suggest that overexpression of PIG11 could induce cell apoptosis in the low levels and enhanced the apoptotic effects of arsenic trioxide. The process could be involved in intracellular generation of ROS.