ArticleHereditas2025
Activation of TRIM37 by ATF6 and degradation of ACSL4: inhibiting ferroptosis and propelling cervical cancer progression.
Article in Hereditas, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers, 1 of them a synthesis that pooled it.
What it found
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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
3 citing papers in PubMed, 1 synthesis or guideline pooled it.
- The interaction between endoplasmic reticulum stress and ferroptosis in ovarian diseases.Journal of ovarian research · 2026Pooled it
- Targeting the unfolded protein response in cancer: mechanisms, small-molecule inhibitors, and translational challenges.Frontiers in immunology · 2026Review
- Long-chain acyl-CoA synthetases: biological functions, diseases and therapeutic targets.Molecular biomedicine · 2025Review
Corrections and comments
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Authors and funding
5 authors.
Funding
Abstract
backgroundCervical cancer (CC), a prevalent gynecological malignancy, shows high global incidence and mortality. Tripartite motif-containing 37 (TRIM37), a significant ubiquitinating enzyme, is overexpressed in CC, fueling its progression, but its role in ferroptosis here is unknown.
methodsTRIM37 expression in CC tissues was first predicted using bioinformatics software. Then, RT-qPCR and Western blot were utilized to confirm TRIM37 expression in CC tissues and cells. Subsequently, cellular behaviors were examined by EdU, flow cytometry, and Transwell assay. Besides, ferroptosis-related indicators were detected by using corresponding kits. The dual luciferase reporter assay was conducted to identify the binding between TRIM37 and Activating Transcription Factor 6 (ATF6). Additionally, the Co-IP assay was applied to validate the interaction between TRIM37 and Acyl-CoA Synthetase Long-Chain Family Member 4 (ACSL4). Finally, the functions of TRIM37 in vivo were investigated by establishing a xenograft tumor model.
resultsTRIM37 expression was increased in CC tissues and cells. Silencing TRIM37 suppressed cell malignant behaviors and promoted ferroptosis. ATF6 activated TRIM37 transcription, with TRIM37 upregulation counteracting ATF6 knockdown effects. TRIM37 degraded ACSL4, and silencing ACSL4 reversed TRIM37 knockdown effects. TRIM37 overexpression counteracted ATF6 knockdown's impact on tumor growth in vivo.
conclusionATF6 regulated the expression of TRIM37, which in turn promoted the ubiquitination and degradation of ACSL4, facilitating the progression of CC.
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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.