Role of ferroptosis and its non-coding RNA regulation in hepatocellular carcinoma

Abstract

Ferroptosis is a newly discovered form of programmed cell death that involves the accumulation of iron-dependent lipid peroxides and plays a vital role in the tumorigenesis, development, and drug resistance of various tumors such as hepatocellular carcinoma (HCC). As a hotspot in molecular biology, non-coding RNAs (ncRNAs) participate in the initiation and progression of HCC, either act as oncogenes or tumor suppressors. Recent studies have shown that ncRNAs can regulate ferroptosis in HCC cells, which would affect the tumor progression and drug resistance. Therefore, clarifying the underlying role of ferroptosis and the regulatory role of ncRNA on ferroptosis in HCC could develop new treatment interventions for this disease. This review briefly summarizes the role of ferroptosis and ferroptosis-related ncRNAs in HCC tumorigenesis, progression, treatment, drug resistance and prognosis, for the development of potential therapeutic strategies and prognostic markers in HCC patients.

The multifaceted perspectives on the regulation of lncRNAs in hepatocellular carcinoma ferroptosis: from bench-to-bedside

“…The GABPB1 protein serves as the activation subunit of the NRF2 transcription factor [ 136 ]. GABPB1 associates with the alpha subunit to form a tetrameric configuration that actively enhances the transcription of a myriad of genes, including those involved in antioxidant defense mechanisms, such as Peroxiredoxin 5 (PRDX5), which is highly expressed in HCC tissues and associates with poor prognosis of patients [ 137 , 138 ]. The lncRNA GABPB1-AS1 is the antisense transcript of GABPB1 mRNA [ 139 ].…”