ArticleCell death & disease2025
NSUN2 mediated-aberrant 5-methylcytosine methylation regulates autophagy-related ferroptosis in oral squamous cell carcinoma progression.
Article in Cell death & disease, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
2 citing papers in PubMed.
- Exploring Ferroptosis: A Key Mechanism in Respiratory System Diseases and its Therapeutic Potential.Applied biochemistry and biotechnology · 2026Review
- Iron homeostasis and macrophage polarization in oral squamous cell carcinoma: mechanisms and therapeutic perspectives.Frontiers in immunology · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
12 authors.
Funding
Abstract
Oral squamous cell carcinoma (OSCC) is a common malignant tumor with high metastasis rates and poor prognosis. This study investigated the role of NOP2/Sun RNA methyltransferase family member 2 (NSUN2), a key 5-methylcytosine (m5C) methyltransferase, and m5C methylation in the progression of OSCC, particularly in relation to ferroptosis resistance. NSUN2 is significantly overexpressed in OSCC tissues and cell lines and its high expression correlates with poor prognosis and aggressive tumor characteristics. Knockdown of NSUN2 in ferroptosis-resistant OSCC cells resulted in increased sensitivity to ferroptosis. Conversely, NSUN2 overexpression conferred ferroptosis resistance, reducing iron accumulation and restoring GPX4 expression even under erastin treatment. Mechanistically, NSUN2 mediates m⁵C modification of sequestosome 1 (SQSTM1)/P62 mRNA, and the m5C reader protein Y-box binding protein 1 (YBX1) enhances SQSTM1/P62 mRNA stability. This regulation suppresses autophagy and thereby inhibits autophagy-dependent ferroptosis in OSCC. In vivo xenograft models confirmed that NSUN2 knockdown significantly inhibited tumorigenicity. Notably, treatment with an autophagy inhibitor (3-MA) or a ferroptosis inhibitor (Fer-1) partially restored tumor growth in NSUN2-knockdown cells, validating the critical role of autophagy and ferroptosis in NSUN2-mediated OSCC progression. These findings identify the NSUN2-YBX1-SQSTM1/P62 axis as a key regulator of autophagy-dependent ferroptosis in OSCC, highlighting NSUN2 as a promising epitranscriptomic target to enhance ferroptosis induction for OSCC therapy.
Indexed as
Identifiers
What Socratic holds
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.