ArticleMolecular and cellular biochemistry2025
SOX11 exacerbates ferroptosis to reduce lenvatinib resistance in liver cancer cells by promoting ubiquitination degradation of SREBF1 through upregulating UBE3A.
Article in Molecular and cellular biochemistry, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed.
- OTUD1-mediated deubiquitination stabilizes SLC7A11 to suppress ferroptosis in hepatocellular carcinoma.Cellular oncology (Dordrecht, Netherlands) · 2026Article
- Sesamin attenuates atherosclerosis by alleviating vascular endothelial ferroptosis-related injuryFrontiers in cell and developmental biology · 2026Article
- Targeting the MIR4435-2HG/miR-29c-3p/FSP1 axis overcomes lenvatinib resistance by inducing ferroptosis in hepatocellular carcinoma.Cancer cell international · 2025Article
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Authors and funding
3 authors.
Funding
Abstract
Lenvatinib is one of the most commonly used first-line drugs for liver cancer. However, lenvatinib resistance occurs in a large proportion of patients, posing a significant challenge. Ferroptosis, an iron-dependent form of cell death, plays a pivotal role in overcoming drug resistance. This study investigates the role of SRY-related HMG-box transcription factor 11 (SOX11) in regulating lenvatinib resistance in liver cancer through its impact on ferroptosis. qRT-PCR, western blot, and immunohistochemistry were performed to examine the expression of key molecules in patient samples and cell lines. Functional studies, including cell viability and proliferation assays, colony formation assays, flow cytometry, and measurements of iron metabolism markers, were conducted to explore the biological effects of these molecules. Additionally, Co-IP, ChIP, dual-luciferase reporter assays, and in vivo tumorigenesis experiments were performed to uncover the underlying regulatory mechanisms. Our results showed that UBE3A was markedly downregulated in lenvatinib-resistant liver cancer tissues and cells, and its overexpression markedly reduced lenvatinib resistance in liver cancer cells by promoting ferroptosis. Mechanically, UBE3A reduced lenvatinib resistance in lenvatinib-resistant liver cancer cells by mediating ubiquitination-independent degradation of SREBF1. In addition, SOX11 upregulation reduced lenvatinib resistance in liver cancer cells by promoting ferroptosis through transcriptionally activated UBE3A expression. In summary, SOX11 upregulation promoted ferroptosis in liver cancer cells by promoting SREBF1 ubiquitination degradation through transcriptionally elevating UBE3A expression, thereby sensitizing lenvatinib-resistant liver cancer cells to lenvatinib.
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Registered trials
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