ArticleCell death discovery2025
TRIM35, a novel DNA-binding protein, epigenetically modifies H3 to promote HSPA6 transcription and suppress breast cancer progression.
Article in Cell death discovery, 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.
- TRIM68 regulates ubiquitinated degradation of Rabex-5 and plays a role in progression of breast cancer through Rab5-Rac1.American journal of cancer research · 2026Article
- HSPA6 Promotes Ferroptosis in Triple-Negative Breast Cancer by Rewiring Lipid Metabolism to Potentiate Membrane Lipid Peroxidation.International journal of biological sciences · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
15 authors.
Funding
Abstract
Tripartite Motif Containing 35 (TRIM35) is a well-characterized ubiquitin ligase with established roles in antiviral immunity, cancer metabolism, cardiovascular function, and tumor progression. However, its function as a DNA-binding protein has not been previously explored. In this study, we provide the first evidence that TRIM35 directly binds genomic promoters, thereby identifying it as a novel regulator of gene transcription. This finding opens new avenues for understanding the biological functions of TRIM35, expanding its potential role in cellular regulation. Furthermore, our results show that TRIM35 interacts with histone H3 (H3) and catalyzes its non-proteolytic ubiquitination, which serves as a recruitment signal for p300, leading to subsequent H3K27 acetylation and activation of gene transcription. Notably, among the genes regulated, Heat Shock Protein Family A (Hsp70) Member 6 (HSPA6) is significantly upregulated through TRIM35-mediated transcriptional regulation, which suppresses breast cancer progression and mediates TRIM35's anti-tumor effect. Collectively, our findings reveal a previously unrecognized mechanism by which TRIM35 regulates gene expression through targeted epigenetic modification, providing new insights into its tumor-suppressive role in breast cancer.
Identifiers
What OpenQuestion 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 OpenQuestion graph.