Renmin Hospital of Jiaozuo

Jiaozuo, China

Renmin Hospital of Jiaozuo

Jiaozuo, China
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Li Z.,Renmin Hospital of Jiaozuo | Li Z.,Central South University | Zhao J.,Central South University | Li Q.,Renmin Hospital of Jiaozuo | And 4 more authors.
Cell Stress and Chaperones | Year: 2010

K562 cells and peripheral blood mononuclear cells were treated with hydrogen peroxide (H2O2) to determine the expression of Krüppel-like factor (KLF) 4. A full-length complementary DNA or an anti-sense oligonucleotide of KLF4 was transfected into cells, and expressions of B-cell lymphoma/leukemia-2 (bcl-2) and bcl-2-associated X (bax) proteins were analyzed. The results showed that H2O2 treatment of cells resulted in an increase in KLF4 levels; KLF4 induced apoptosis and slowed cell growth, potentially resulting from up-regulation of bax and down-regulation of bcl-2. Transcriptional activities on bcl-2 and bax were promoted following KLF4 overexpression potentially through KLF4 binding sites on corresponding promoters. All results indicate that KLF4 induces apoptosis in leukemia cells involving the bcl-2/bax pathway during H2O2 stimulation, suggesting a potential mechanism for research on drug-induced apoptosis. © 2010 Cell Stress Society International.


PubMed | Renmin Hospital of Jiaozuo
Type: Journal Article | Journal: Cell stress & chaperones | Year: 2010

K562 cells and peripheral blood mononuclear cells were treated with hydrogen peroxide (H(2)O(2)) to determine the expression of Krppel-like factor (KLF) 4. A full-length complementary DNA or an anti-sense oligonucleotide of KLF4 was transfected into cells, and expressions of B-cell lymphoma/leukemia-2 (bcl-2) and bcl-2-associated X (bax) proteins were analyzed. The results showed that H(2)O(2) treatment of cells resulted in an increase in KLF4 levels; KLF4 induced apoptosis and slowed cell growth, potentially resulting from up-regulation of bax and down-regulation of bcl-2. Transcriptional activities on bcl-2 and bax were promoted following KLF4 overexpression potentially through KLF4 binding sites on corresponding promoters. All results indicate that KLF4 induces apoptosis in leukemia cells involving the bcl-2/bax pathway during H(2)O(2) stimulation, suggesting a potential mechanism for research on drug-induced apoptosis.

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