CircDCBLD2 alleviates liver fibrosis by regulating ferroptosis via facilitating STUB1-mediated PARK7 ubiquitination degradation

Wang, Juan; Zhang, Haoye; Chen, Limin; Fu, Kangkang; Yan, Yu; Liu, Zhenguo

doi:10.1007/s00535-023-02068-6

J Gastroenterol

2024

DOI: 10.1007/s00535-023-02068-6

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CircDCBLD2 alleviates liver fibrosis by regulating ferroptosis via facilitating STUB1-mediated PARK7 ubiquitination degradation

Juan Wang,

Haoye Zhang,

Limin Chen

et al.

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2024

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Cited by 2 publications

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STUB1 promotes the degradation of HSPB1 and induces ferroptosis in lung cancer cells

Tieliwaerdi,

Aini,

Amuti

et al. 2024

Environmental Toxicology

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Lung cancer is a common malignancy characterized by ferroptosis, an iron‐dependent form of cell death caused by excessive lipid peroxidation. The disruption of the ubiquitination system plays a crucial role in tumor development and spread. In recent years, there has been increasing interest in utilizing ferroptosis for lung cancer treatment; however, the precise mechanism of how ubiquitination modulates ferroptosis remains unclear. We used databases to analyze STUB1 expression patterns in lung cancer tissues compared to normal tissues and performed immunohistochemistry. The functional role of STUB1 was investigated through gain‐of‐function and loss‐of‐function experiments both in vitro and in vivo. Malondialdehyde levels, Fe2+ content, and cell viability assays were employed to evaluate ferroptosis status. Downstream targets of STUB1 were identified through screening and validated using immunoprecipitation and ubiquitination assays. Our findings demonstrate that STUB1 is downregulated in lung cancer cells and functions as an inhibitor of their growth and metastasis both in vitro and in vivo while promoting ferroptosis. Mechanistically, STUB1 induces ferroptosis through E3 ligase‐dependent degradation of the ferroptosis suppressor HSPB1. Furthermore, our study elucidated the specific types and sites of modification on HSPB1 mediated by STUB1. This research establishes STUB1 as a tumor suppressor influencing proliferation of lung cancer cells as well as the epithelial‐mesenchymal transition process associated with it. Importantly, our work highlights the role of STUB1 in ubiquitination‐mediated degradation of HSPB1, providing insights for potential treatments for lung cancer.

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STUB1 promotes the degradation of HSPB1 and induces ferroptosis in lung cancer cells

Tieliwaerdi,

Aini,

Amuti

et al. 2024

Environmental Toxicology

View full text Add to dashboard Cite

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The role of ferroptosis-related non-coding RNA in liver fibrosis

Zhang,

Wu,

Jiang

et al. 2024

Front. Cell Dev. Biol.

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Liver fibrosis represents a reversible pathophysiological process, caused by chronic inflammation stemming from hepatocyte damage. It delineates the initial stage in the progression of chronic liver disease. This pathological progression is characterized by the excessive accumulation of the extracellular matrix (ECM), which leads to significant structural disruption and ultimately impairs liver function. To date, no specific antifibrotic drugs have been developed, and advanced liver fibrosis remains largely incurable. Liver transplantation remains the sole efficacious intervention for advanced liver fibrosis; nevertheless, it is constrained by exorbitant costs and the risk of postoperative immune rejection, underscoring the imperative for novel therapeutic strategies. Ferroptosis, an emergent form of regulated cell death, has been identified as a pivotal regulatory mechanism in the development of liver fibrosis and is intricately linked with the progression of liver diseases. Recent investigations have elucidated that a diverse array of non-coding RNAs (ncRNAs), including microRNAs, long non-coding RNAs, and circular RNAs, are involved in the ferroptosis pathway, thereby modulating the progression of various diseases, including liver fibrosis. In recent years, the roles of ferroptosis and ferroptosis-related ncRNAs in liver fibrosis have attracted escalating scholarly attention. This paper elucidates the pathophysiology of liver fibrosis, explores the mechanisms underlying ferroptosis, and delineates the involvement of ncRNA-mediated ferroptosis pathways in the pathology of liver fibrosis. It aims to propose novel strategies for the prevention and therapeutic intervention of liver fibrosis.

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CircDCBLD2 alleviates liver fibrosis by regulating ferroptosis via facilitating STUB1-mediated PARK7 ubiquitination degradation

Cited by 2 publications

References 56 publications

STUB1 promotes the degradation of HSPB1 and induces ferroptosis in lung cancer cells

STUB1 promotes the degradation of HSPB1 and induces ferroptosis in lung cancer cells

The role of ferroptosis-related non-coding RNA in liver fibrosis

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