Emerging insights into the role of microRNAs regulation of ferroptosis in hepatocellular carcinoma

IF 4.2 2区生物学 Q2 BIOCHEMISTRY & MOLECULAR BIOLOGY

Biochimica et biophysica acta. Molecular basis of disease Pub Date : 2024-12-27 DOI:10.1016/j.bbadis.2024.167642

Qi Zhang, Yingdan Zhang, Shiyun Guo, Honggang Wang

引用次数: 0

Abstract

Hepatocellular carcinoma (HCC) is a major type of liver cancer and an important cause of cancer death. It has been reported that the hepatocyte death plays an important role in HCC. Ferroptosis is an iron-dependent programmed cell death characterized by the accumulation of free iron and lipid peroxidation. A series of studies have shown that ferroptosis contributes to the occurrence and development of HCC. MicroRNAs (miRNAs) are non-coding RNAs with a length of approximately 222 nt. In recent years, miRNAs have been shown to participate in regulating ferroptosis to play a vital role in HCC, but the related mechanisms are not fully understood. This review summarized the current understanding of ferroptosis, as well as the biogenesis and function of miRNAs, and focused on the role of miRNAs regulation of ferroptosis in HCC, with the hope of providing new targets and ideas for the treatment of HCC.

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在肝细胞癌中微rna调控铁下垂作用的新见解。

肝细胞癌（HCC）是肝癌的主要类型，也是癌症死亡的重要原因。有报道称肝细胞死亡在HCC中起重要作用。铁死亡是一种铁依赖性程序性细胞死亡，其特征是游离铁的积累和脂质过氧化。一系列研究表明，铁下垂有助于HCC的发生和发展。MicroRNAs （miRNAs）是长度约为21-22 nt的非编码rna。近年来，mirna参与调节铁下垂在HCC中发挥重要作用，但相关机制尚不完全清楚。本文综述了目前对铁下垂的认识，以及mirna的生物发生和功能，重点讨论了mirna在HCC中对铁下垂的调控作用，希望为HCC的治疗提供新的靶点和思路。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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来源期刊

Biochimica et biophysica acta. Molecular basis of disease 生物-生化与分子生物学

CiteScore

12.30

自引率

0.00%

发文量

218

审稿时长

32 days

期刊介绍： BBA Molecular Basis of Disease addresses the biochemistry and molecular genetics of disease processes and models of human disease. This journal covers aspects of aging, cancer, metabolic-, neurological-, and immunological-based disease. Manuscripts focused on using animal models to elucidate biochemical and mechanistic insight in each of these conditions, are particularly encouraged. Manuscripts should emphasize the underlying mechanisms of disease pathways and provide novel contributions to the understanding and/or treatment of these disorders. Highly descriptive and method development submissions may be declined without full review. The submission of uninvited reviews to BBA - Molecular Basis of Disease is strongly discouraged, and any such uninvited review should be accompanied by a coverletter outlining the compelling reasons why the review should be considered.