ArticleCell death & disease2024
SNF2L maintains glutathione homeostasis by initiating SLC7A11 transcription through chromatin remodeling.
Article in Cell death & disease, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers, 2 of them syntheses that pooled it.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
5 citing papers in PubMed, 2 syntheses or guidelines pooled it.
- xCT (Slc7a11) Regulation: Lessons from Cancer Research.Neurochemical research · 2026Pooled it
- Metabolomic insights into late-life depression: a systematic review.BMC geriatrics · 2025Pooled it
- Identifying breast cancer subtypes and exploring spatial expression patterns of the key subtype-specific gene based on pathological images, single-cell sequencing, and spatial transcriptomic data.Breast cancer (Tokyo, Japan) · 2026Article
- The roles of chromatin remodeling and 3D genome organization in cancers: from mechanistic insights to emerging treatment options.Molecular cancer · 2026Review
- DNA-damage dependent interaction of Orc6 to SMARCA1 in S-phase modulates chromatin remodeling.Nucleic acids research · 2026Article
Corrections and comments
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Authors and funding
11 authors.
Funding
Abstract
SNF2L encodes an ISWI chromatin remodeling factor that promotes gene transcription and is consistently elevated in cancers. Previous studies have shown that inhibiting SNF2L expression in cancer cells leads to significant growth suppression, DNA damage, and cell death. However, the underlying mechanisms remain poorly understood. In this study, we demonstrated that cancer cells lacking SNF2L show significantly decreased glutathione (GSH) levels, leading to elevated reactive oxygen species (ROS) and increased oxidative stress. SNF2L deficiency also heightened the sensitivity of cancer cells to APR-246, a drug that depletes GSH and induces oxidative stress, consequently decreasing cell viability and increasing ROS levels, regardless of p53 status. Mechanistically, we found that NRF2 recruits SNF2L to the SLC7A11 promoter, leading to increased chromatin accessibility and facilitating SLC7A11 transcription. This results in decreased cystine uptake and impaired GSH biosynthesis. These findings suggest that targeting the SNF2L/SLC7A11 axis could enhance the effectiveness of APR-246 by depleting GSH and increasing ROS level in cancer cells, highlighting SNF2L as a promising therapeutic target.
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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 Socratic graph.