Abstract:
Epitranscriptomics is a field that delves into post-transcriptional changes. Among these modifications, the conversion of adenosine to inosine, traduced as guanosine (A>I(G)), is one of the known RNA-editing mechanisms, catalyzed by ADARs. This type of RNA editing is the most common type of editing in mammals and contributes to biological diversity. Disruption in the A>I(G) RNA-editing balance has been linked to diseases, including several types of cancer. Drug resistance in patients with cancer represents a significant public health concern, contributing to increased mortality rates resulting from therapy non-responsiveness and disease progression, representing the greatest challenge for researchers in this field. The A>I(G) RNA editing is involved in several mechanisms over the immunotherapy and genotoxic drug response and drug resistance. This review investigates the relationship between ADAR1 and specific A>I(G) RNA-edited sites, focusing particularly on breast cancer, and the impact of these sites on DNA damage repair and the immune response over anti-cancer therapy. We address the underlying mechanisms, bioinformatics, and in vitro strategies for the identification and validation of A>I(G) RNA-edited sites. We gathered databases related to A>I(G) RNA editing and cancer and discussed the potential clinical and research implications of understanding A>I(G) RNA-editing patterns. Understanding the intricate role of ADAR1-mediated A>I(G) RNA editing in breast cancer holds significant promise for the development of personalized treatment approaches tailored to individual patients\' A>I(G) RNA-editing profiles.
摘要:
外写是一个研究转录后变化的领域。在这些修改中,腺苷转化为肌苷,作为鸟苷(A>I(G)),是已知的RNA编辑机制之一,由ADAR催化。这种类型的RNA编辑是哺乳动物中最常见的编辑类型,有助于生物多样性。A>I(G)RNA编辑平衡的破坏与疾病有关,包括几种癌症。癌症患者的耐药性是一个重要的公共卫生问题,导致治疗无反应性和疾病进展导致的死亡率增加,代表了这一领域研究人员的最大挑战。A>I(G)RNA编辑涉及免疫疗法和基因毒性药物反应和耐药性的几种机制。这篇综述研究了ADAR1与特定A>I(G)RNA编辑位点之间的关系,特别关注乳腺癌,以及这些位点对DNA损伤修复和抗癌治疗的免疫反应的影响。我们解决了潜在的机制,生物信息学,以及鉴定和验证A>I(G)RNA编辑位点的体外策略。我们收集了与A>I(G)RNA编辑和癌症相关的数据库,并讨论了理解A>I(G)RNA编辑模式的潜在临床和研究意义。了解ADAR1介导的A>I(G)RNA编辑在乳腺癌中的复杂作用,对于开发针对个体患者的个性化治疗方法具有重要意义。