Abstract:
:Stathmin is overexpressed in a variety of assessed human malignancies and is correlated with tumor progression and poor prognosis. Downregulation of its expression will contribute to optimize therapeutic outcomes in the treatment of various malignancies. However, the mechanisms of stathmin gene overexpression are not completely elucidated at present. Early growth response 1 (Egr1) is a transcription factor that triggers transcription of downstream genes mediating cell growth and angiogenesis upon various stimulations. Following the previous computational identification of a site that was thought to be an Egr1 consensus binding sequence at -85 to -94 region in stathmin gene promoter, we analyzed the role of Egr1 in the regulation of stathmin gene expression in lung cancer cell line A549. The results showed that Egr1 transcription factor bound to the sequence 5'-GCGGGGGCG-3' within human stathmin gene promoter; and in reporter gene assays and overexpression experiments, both stathmin gene promoter activity and stathmin gene expression level were downregulated following endogenous or exogenous expression of Egr1. Using wild type Egr1 and knockout Egr1 cell lines, we demonstrated that p53 negatively regulates stathmin expression through Egr1 pathway. In summary, Egr1 is a novel regulator of stathmin expression and p53 mediates the transcriptional repression of stathmin by Egr1 in human lung cancer cells.
journal_name
Cell Signaljournal_title
Cellular signallingauthors
Fang L,Min L,Lin Y,Ping G,Rui W,Ying Z,Xi W,Ting H,Li L,Ke D,Jihong R,Huizhong Zdoi
10.1016/j.cellsig.2009.09.030subject
Has Abstractpub_date
2010-01-01 00:00:00pages
166-73issue
1eissn
0898-6568issn
1873-3913pii
S0898-6568(09)00280-0journal_volume
22pub_type
杂志文章abstract::Deficits in brain function that are associated with aging and age-related diseases benefit very little from currently available therapies, suggesting a better understanding of the underlying molecular mechanisms is needed to develop improved drugs. Here, we review the literature to test the hypothesis that a break dow...
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journal_title:Cellular signalling
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abstract::Cellular hypoxia can lead to cell death or adaptation and has important effects on development, physiology, and pathology. Here, we investigated the role and regulation of ceramide in hypoxia-induced apoptosis of SH-SY5Y neuroblastoma cells. Hypoxia increased the ceramide concentration; subsequently, we observed bioch...
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更新日期:2010-04-01 00:00:00
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journal_title:Cellular signalling
pub_type: 杂志文章,评审
doi:10.1016/s0898-6568(96)00101-5
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更新日期:2013-10-01 00:00:00
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journal_title:Cellular signalling
pub_type: 杂志文章,评审
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abstract::Hydrogen peroxide (H(2)O(2)) mediates induction of cytotoxicity in various cell types. GSK-3beta has been found to participate in a number of signaling pathways, including cell proliferation and cell death. In the present study, we show that GSK-3beta is rapidly dephosphorylated and activated in response to H(2)O(2) t...
journal_title:Cellular signalling
pub_type: 杂志文章
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更新日期:2006-05-01 00:00:00
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journal_title:Cellular signalling
pub_type: 杂志文章,评审
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更新日期:2016-08-01 00:00:00
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journal_title:Cellular signalling
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journal_title:Cellular signalling
pub_type: 杂志文章
doi:10.1016/j.cellsig.2013.11.019
更新日期:2014-02-01 00:00:00
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journal_title:Cellular signalling
pub_type: 杂志文章
doi:10.1016/j.cellsig.2009.04.006
更新日期:2009-09-01 00:00:00
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journal_title:Cellular signalling
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doi:10.1016/j.cellsig.2018.01.014
更新日期:2018-04-01 00:00:00
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doi:10.1016/j.cellsig.2017.09.005
更新日期:2018-01-01 00:00:00
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pub_type: 杂志文章
doi:10.1016/s0898-6568(01)00205-4
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journal_title:Cellular signalling
pub_type: 杂志文章,评审
doi:10.1016/s0898-6568(98)00059-x
更新日期:1999-04-01 00:00:00
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journal_title:Cellular signalling
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doi:10.1016/j.cellsig.2012.03.009
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journal_title:Cellular signalling
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doi:10.1016/j.cellsig.2007.01.010
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journal_title:Cellular signalling
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journal_title:Cellular signalling
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更新日期:2014-02-01 00:00:00
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journal_title:Cellular signalling
pub_type: 杂志文章,评审
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更新日期:1996-08-01 00:00:00
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journal_title:Cellular signalling
pub_type: 杂志文章
doi:10.1016/j.cellsig.2005.07.006
更新日期:2006-06-01 00:00:00
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journal_title:Cellular signalling
pub_type: 杂志文章,收录出版
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更新日期:2016-11-01 00:00:00
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journal_title:Cellular signalling
pub_type: 杂志文章,评审
doi:10.1016/j.cellsig.2020.109816
更新日期:2021-01-01 00:00:00
abstract::Mice lacking the gene for suppressor of cytokine signaling 1 (SOCS1) show defective homeostasis of T lymphocytes due to accumulation of CD8(+) T cells, resulting at least partly from dysregulated IL-15 signaling. IL-15 alone does not stimulate proliferation of naïve CD8 T cells, but can synergize with IL-21 to induce ...
journal_title:Cellular signalling
pub_type: 杂志文章
doi:10.1016/j.cellsig.2006.10.003
更新日期:2007-04-01 00:00:00
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journal_title:Cellular signalling
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更新日期:1997-09-01 00:00:00