ArticleCell death discovery2024
MDH2 regulates the sensitivity of clear cell renal cell carcinoma to ferroptosis through its interaction with FSP1.
Article in Cell death discovery, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
What it found
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The trial behind it
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Who cites it
8 citing papers in PubMed.
- Ferroptosis in renal cell carcinoma: integrative multi-omics insights and therapeutic perspectives.International journal of surgery (London, England) · 2026Article
- The role of ferroptosis in renal cell carcinoma: molecular mechanisms and therapeutic implications.Journal of molecular medicine (Berlin, Germany) · 2026Review
- Ferroptosis-Mediated Cell-Specific Damage: Molecular Cascades and Therapeutic Breakthroughs in Diabetic Retinopathy.Antioxidants (Basel, Switzerland) · 2025Review
- Lipid reprogramming and ferroptosis crosstalk in clear cell renal cell carcinoma: metabolic vulnerabilities and therapeutic targeting.Molecular cancer · 2025Review
- The cancer-induced lactate load and oncologic remodeling hypothesis: lactate as a driver of biosynthesis and epigenetics in cancer.Frontiers in oncology · 2025Article
- PRMT5-Mediated Arginine Methylation of ACSL4 Attenuates Its Stability and Suppresses Ferroptosis in Renal Cancer.Research (Washington, D.C.) · 2025Article
- NEDD4L Suppresses Proliferation and Promotes Apoptosis by Ubiquitinating RAC2 Expression and Acts as a Prognostic Biomarker in Clear Cell Renal Cell Carcinoma.International journal of molecular sciences · 2024Article
- Ferroptosis-associated genes and compounds in renal cell carcinoma.Frontiers in immunology · 2024Review
Corrections and comments
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Authors and funding
7 authors.
Funding
Abstract
Malate dehydrogenase 2 is a pivotal enzyme in the tricarboxylic acid cycle. Recent studies have highlighted the significant involvement of MDH2 in the pathogenesis and progression of diverse types of tumors, yet its precise mechanistic underpinnings remain elusive. This study revealed a significant decrease in MDH2 expression in renal cancer tissues. And knocking out MDH2 was observed to hinder the proliferation of normal renal tubular epithelial cells but notably enhance the proliferation of ccRCC. Furthermore, mechanistically, we found that MDH2 inhibits the proliferation of ccRCC by promoting ferroptosis, while enhancing the sensitivity of ccRCC to ferroptosis inducers, promoting lipid peroxidation. We also demonstrated that MDH2 regulates the ubiquitination of FSP1 through protein-protein interactions, leading to a decrease in FSP1 protein levels and maintaining high sensitivity of ccRCC to ferroptosis. In conclusion, our study demonstrates that the reduced MDH2 expression in ccRCC results in increased expression of FSP1, thereby reducing its sensitivity to ferroptosis. It unveils a non-metabolic role for the downregulation of MDH2 in ccRCC progression.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.