Literature DB >> 19792968

Is EGR1 a potential target for prostate cancer therapy?

Delphine Gitenay1, Véronique T Baron.   

Abstract

Prostate cancer is a major cause of cancer-related death in American men, for which finding new therapeutic strategies remains a challenge. Early growth response-1 (EGR1) is a transcription factor involved in cell proliferation and in the regulation of apoptosis. Although it has long been considered a tumor suppressor, a wealth of new evidence shows that EGR1 promotes the progression of prostate cancer. This review addresses the paradoxes of EGR1 function. While EGR1 mediates apoptosis in response to stress and DNA damage by regulating a tumor suppressor network, it also promotes the proliferation of prostate cancer cells by a mechanism that is not fully understood. Thus, EGR1 might be targeted for prostate cancer therapy either by ectopic expression in combination with radiotherapy or chemotherapy, or by direct inhibition for systemic treatment. Possible strategies to antagonize EGR1 function in a therapeutic setting are discussed.

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Year:  2009        PMID: 19792968      PMCID: PMC2776080          DOI: 10.2217/fon.09.67

Source DB:  PubMed          Journal:  Future Oncol        ISSN: 1479-6694            Impact factor:   3.404


  98 in total

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  60 in total

1.  Age-associated up-regulation of EGR1 promotes granulosa cell apoptosis during follicle atresia in mice through the NF-κB pathway.

Authors:  Suzhen Yuan; Jingyi Wen; Jing Cheng; Wei Shen; Su Zhou; Wei Yan; Lu Shen; Aiyue Luo; Shixuan Wang
Journal:  Cell Cycle       Date:  2016-07-19       Impact factor: 4.534

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Journal:  Clin Cancer Res       Date:  2013-07-09       Impact factor: 12.531

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Journal:  Prostate       Date:  2011-11-29       Impact factor: 4.104

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Journal:  Cancer Cell       Date:  2011-05-27       Impact factor: 31.743

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Authors:  Kai-Cheng Chuang; Fan-Wen Chen; Meng-Hsiun Tsai; Jeng-Jer Shieh
Journal:  Oncol Lett       Date:  2021-02-19       Impact factor: 2.967

8.  Malignant transformation of CD4+ T lymphocytes mediated by oncogenic kinase NPM/ALK recapitulates IL-2-induced cell signaling and gene expression reprogramming.

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Authors:  Bin Guo; Xue-Chao Tian; Dang-Dang Li; Zhan-Qing Yang; Hang Cao; Qiao-Ling Zhang; Ju-Xiong Liu; Zhan-Peng Yue
Journal:  Cell Cycle       Date:  2014       Impact factor: 4.534

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Authors:  L Sauer; D Gitenay; C Vo; V T Baron
Journal:  Oncogene       Date:  2010-03-01       Impact factor: 9.867

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