TRIM47-CDO1 axis dictates hepatocellular carcinoma progression by modulating ferroptotic cell death through the ubiquitin‒proteasome system
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View abstract on PubMed
Summary
This summary is machine-generated.Tripartite motif-containing protein 47 (TRIM47) promotes hepatocellular carcinoma (HCC) growth and spread. Targeting TRIM47 may offer new therapeutic strategies for liver cancer by inducing ferroptosis via CDO1 regulation.
Area Of Science
- Oncology
- Molecular Biology
- Biochemistry
Background
- Hepatocellular carcinoma (HCC) presents significant global health challenges due to high mortality and limited treatment options.
- Tripartite motif-containing protein 47 (TRIM47), an E3 ubiquitin ligase, is implicated in disease progression, but its role in HCC is not fully understood.
Purpose Of The Study
- To elucidate the specific mechanisms by which TRIM47 influences hepatocellular carcinoma development and progression.
- To investigate the potential of TRIM47 as a therapeutic target in HCC treatment.
Main Methods
- Analysis of TRIM47 expression in HCC tumor tissues and correlation with clinical parameters.
- In vitro gain- and loss-of-function experiments to assess TRIM47's impact on HCC cell proliferation, migration, and invasion.
- Investigation of TRIM47's role in ferroptosis induction, focusing on its interaction with CDO1 and regulation of glutathione (GSH) synthesis.
Main Results
- TRIM47 expression is elevated in HCC tissues and correlates with advanced clinical staging and poorer patient prognosis.
- TRIM47 overexpression enhances HCC cell proliferation, migration, and invasion, while its knockdown induces ferroptosis.
- TRIM47 interacts with CDO1, promoting its K48-linked ubiquitination and subsequent degradation, which impairs GSH synthesis and triggers ferroptosis.
- CDO1 antagonizes the oncogenic effects of TRIM47 in HCC cells.
Conclusions
- TRIM47 acts as an oncogene in HCC, promoting tumor progression and inhibiting ferroptosis through the ubiquitination and degradation of CDO1.
- TRIM47's mechanism involving CDO1-mediated ferroptosis offers a novel therapeutic avenue for hepatocellular carcinoma.
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