Induction of p73β by a naphthoquinone analog is mediated by E2F‐1 and triggers apoptosis in HeLa cells
Induction of p73β by a naphthoquinone analog is mediated by E2F‐1 and triggers apoptosis in HeLa cells
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E2F-1 介导萘醌类似物诱导 p73β 并引发 HeLa 细胞凋亡
DOI：
10.1016/s0014-5793(02)02921-6
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发表时间：
2002
期刊：
影响因子：
3.5
通讯作者：
Kyunghee Choi
中科院分区：
文献类型：
--
作者：
K. Kang;Jung;Keun;S. Ham;M. Kim;Kyunghee Choi
Recently, p73 was identified as a structural and functional homolog of p53. The p73 protein activates the transcription of genes downstream of p53 and induces apoptosis when overexpressed in several cell lines, similar to the tumor suppressor p53. However, the extracellular stimuli and molecular mechanisms regulating p73 activity remain to be elucidated. In this paper, we present evidence that the naphthoquinone analog, 2,3-dichloro-5,8-dihydroxy-1,4-naphthoquinone (NA), is a novel apoptotic stimulus that induces p73β expression. Treatment with NA induced the expression of p73β mRNA and protein and its downstream genes, p21 and bax, in HeLa cells. Similar results were obtained in MCF7 cells (p53+/+, p73+/+). In the MCF7 cells, p53 protein level was rather decreased by NA treatment. Overexpression of p73β led to the apoptosis of HeLa cells and enhancement of NA-induced cell death. Expression of p73β was mediated by E2F-1, which was activated via release from pRB after exposure of cells to NA. We additionally observed that overexpression of pRB inhibited NA-induced apoptosis. These results imply that p53-independent p73β-dependent p21 expression is involved in NA-induced apoptosis of HeLa cells.
影响因子：
11.2
作者：
Jian‐hui Zhu;Jieyuan Jiang;Wenjing Zhou;Xinbin Chen
通讯作者：
Jian‐hui Zhu;Jieyuan Jiang;Wenjing Zhou;Xinbin Chen