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miR-1-3p 在癌症中的重要作用。

The important role of miR-1-3p in cancers.

机构信息

Department of Pharmacy, School of Pharmacy, Phase I Clinical Trial Centre, The Affiliated Changsha Central Hospital, Hengyang Medical School, University of South China, Changsha, China.

Hunan Provincial Key Laboratory of Tumor Microenvironment Responsive Drug Research, Hengyang, China.

出版信息

J Transl Med. 2023 Oct 31;21(1):769. doi: 10.1186/s12967-023-04649-8.

Abstract

Cancer is a malignant tumor that seriously threatens human life and health. At present, the main treatment methods include surgical resection, chemotherapy, radiotherapy, and immunotherapy. However, the mechanism of tumor occurrence and development is complex, and it produces resistance to some traditional treatment methods, leading to treatment failure and a high mortality rate for patients. Therefore, exploring the molecular mechanisms of tumor occurrence, development, and drug resistance is a very important task. MiRNAs are a type of non-coding small RNA that regulate a series of biological effects by binding to the 3'-UTR of the target mRNA, degrading the mRNA, or inhibiting its translation. MiR-1-3p is an important member of them, which is abnormally expressed in various tumors and closely related to the occurrence and development of tumors. This article introduces miR-1-3p from multiple aspects, including its production and regulation, role in tumor occurrence and development, clinical significance, role in drug resistance, and approaches for targeting miR-1-3p. Intended to provide readers with a comprehensive understanding of the important role of miR-1-3p in tumors.

摘要

癌症是严重威胁人类生命健康的恶性肿瘤。目前,主要的治疗方法包括手术切除、化疗、放疗和免疫治疗。然而,肿瘤发生发展的机制复杂,对一些传统治疗方法产生耐药性,导致治疗失败和患者死亡率高。因此,探索肿瘤发生、发展和耐药的分子机制是非常重要的任务。miRNAs 是一类非编码的小 RNA,通过与靶 mRNA 的 3'-UTR 结合,降解 mRNA 或抑制其翻译,来调节一系列的生物学效应。miR-1-3p 是其中的重要成员,在各种肿瘤中异常表达,与肿瘤的发生发展密切相关。本文从 miR-1-3p 的产生和调控、在肿瘤发生发展中的作用、临床意义、在耐药中的作用以及针对 miR-1-3p 的靶向方法等多个方面进行介绍,旨在为读者提供对 miR-1-3p 在肿瘤中重要作用的全面认识。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d16a/10617136/faaa64e1a412/12967_2023_4649_Fig1_HTML.jpg

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