摘要
背景技术:Aldo-keto还原酶1C3(AKR1C3)是具有多种底物的重要氧化还原酶,涉及产生睾丸内雄激素。其活动受环境暴露以及遗传变异的影响。因此,这些遗传变异体可以产生可变的睾酮水平和随后的雄激素受体(AR)活化。这可能导致前列腺特异性抗原(PSA)的下游产生差异。由于PSA水平用于前列腺的临床评估,这些变化可能会影响前列腺癌(PC)诊断以及PC管理结果。本综述汇集了关于该酶的关键功能,其在PC中的相关性,其转录调节,与遗传学相关的临床方面,癌症和癌症进展中的差异调节以及具有未来治疗价值的AKR1C3抑制剂的类型的信息。 结论:在这些讨论的基础上,提出了在PC中转化医学实践中该酶及其遗传变体的未来适用性的假设。还讨论了使用个性化AKR1C3抑制剂药物用于晚期PC的选择。
关键词: AKR1C3 rs 12529,睾丸外雄激素,前列腺特异性抗原(PSA),前列腺癌(PC),癌症进展,雄激素剥夺治疗(ADT),AKR1C3抑制剂。
图形摘要
Current Cancer Drug Targets
Title:Influence of Aldo-keto Reductase 1C3 in Prostate Cancer - A Mini Review
Volume: 17 Issue: 7
关键词: AKR1C3 rs 12529,睾丸外雄激素,前列腺特异性抗原(PSA),前列腺癌(PC),癌症进展,雄激素剥夺治疗(ADT),AKR1C3抑制剂。
摘要: Background: Aldo-keto reductase 1C3 (AKR1C3) is an important oxidoreductase with multiple substrates, that are involved in producing extra-testicular androgens. Its activity is influenced by environmental exposures, as well as by genetic variants. These genetic variants could therefore produce variable testosterone levels and subsequent androgen receptor (AR) activation. This could lead to differential downstream production of the prostate-specific antigen (PSA). As PSA level is used for clinical evaluation of the prostate, these variations could impact prostate cancer (PC) diagnosis, as well as PC management outcomes. This review brings together information with regards to key functions of this enzyme, its relevance in PC, its transcriptional regulation, clinical aspects associated with genetics, differential regulation in cancer and cancer progression, and the types of AKR1C3 inhibitors with future therapeutic value.
Conclusion: Based on these discussions, hypotheses are forwarded for future applicability of this enzyme and its genetic variants in transformational medical practices in PC. Options for the use of personalised AKR1C3 inhibitor drugs for late stage PC are also discussed.Export Options
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Cite this article as:
Influence of Aldo-keto Reductase 1C3 in Prostate Cancer - A Mini Review, Current Cancer Drug Targets 2017; 17 (7) . https://dx.doi.org/10.2174/1568009617666170330115722
DOI https://dx.doi.org/10.2174/1568009617666170330115722 |
Print ISSN 1568-0096 |
Publisher Name Bentham Science Publisher |
Online ISSN 1873-5576 |
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