Gitenay Delphine, Baron Véronique T
The Vaccine Research Institute of San Diego, San Diego, CA 92121, USA. 19429708
Future Oncol. 2009 Sep;5(7):993-1003. doi: 10.2217/fon.09.67.
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.
前列腺癌是美国男性癌症相关死亡的主要原因，寻找新的治疗策略仍然是一项挑战。早期生长反应因子1（EGR1）是一种参与细胞增殖和细胞凋亡调节的转录因子。尽管长期以来它一直被认为是一种肿瘤抑制因子，但大量新证据表明EGR1促进前列腺癌的进展。本综述阐述了EGR1功能的矛盾之处。虽然EGR1通过调节肿瘤抑制网络介导应激和DNA损伤后的细胞凋亡，但它也通过一种尚未完全了解的机制促进前列腺癌细胞的增殖。因此，EGR1可通过与放疗或化疗联合的异位表达，或通过直接抑制进行全身治疗，作为前列腺癌治疗的靶点。文中讨论了在治疗环境中拮抗EGR1功能的可能策略。
