USP11 is involved in the sensitivity of liver cancer cells to ferroptosis and taxanes through the regulation of NRF2 ubiquitin-mediated degradation
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View abstract on PubMed
Summary
This summary is machine-generated.Ubiquitin-specific protease 11 (USP11) promotes hepatocellular carcinoma (HCC) progression by inhibiting ferroptosis and taxane sensitivity. USP11 targets NRF2, representing a potential therapeutic target for HCC treatment.
Area Of Science
- Oncology
- Molecular Biology
- Biochemistry
Background
- Ubiquitin-specific protease 11 (USP11) is implicated in tumor progression.
- Its role in hepatocellular carcinoma (HCC) ferroptosis and taxane sensitivity is unclear.
Purpose Of The Study
- To investigate the effects of USP11 on ferroptosis and taxane sensitivity in HCC.
- To elucidate the underlying mechanisms of USP11 action in HCC.
Main Methods
- Analysis of HCC clinical specimens and cell lines.
- Gene and protein expression analysis (RT-qPCR, Western blotting, IHC).
- Assessment of cell proliferation, migration, invasion, and ferroptosis indices (Fe2+, GSH, MDA, ROS).
Main Results
- USP11 is upregulated in HCC and promotes proliferation, migration, and invasion.
- USP11 overexpression inhibits ferroptosis by increasing GSH, SLC7A11, and GPX4, and decreasing Fe2+, MDA, and ROS.
- USP11 overexpression reduces sensitivity to taxanes (paclitaxel, docetaxel, cabazitaxel).
Conclusions
- USP11 plays a critical role in regulating ferroptosis and drug resistance in HCC.
- USP11 enhances NRF2 expression via deubiquitination, contributing to reduced ferroptosis and taxane sensitivity.
- USP11 is identified as a potential therapeutic target for HCC treatment.
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