ArticleCancer cell international2026
Integrating bioinformatic analyses and experimental validation of disulfidptosis-related genes and TMX4 in melanoma progression.
Article in Cancer cell international, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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
1 citing paper in PubMed.
- Disulfidptosis: Mechanisms, evidence boundaries, and translational opportunities.Redox biology · 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
6 authors.
Funding
Abstract
backgroundMelanoma is a highly metastatic and lethal malignancy originating from melanocytes. Disulfidptosis is a recently discovered type of programmed cell death with promising potential in cancer therapy. This study aims to establish a prognostic risk model based on disulfidptosis-related gene signatures and investigate their roles in melanoma progression. MATERIALS AND
methodsTranscriptomic data from the TCGA-SKCM and GEO databases were analyzed to identify disulfidptosis-related gene expression profiles in melanoma. Consensus clustering categorized samples into two molecular subtypes, followed by comprehensive analyses of genomic and immune infiltration characteristics. A prognostic risk model was developed using Lasso regression based on DEGs. The expression and function of TMX4 were further validated using IHC and in vitro experiments, including siRNA-mediated knockdown in A375 and A875 melanoma cell lines. Cell proliferation, migration, and indicators of redox homeostasis (GSH, MDA, and ROS) were evaluated, and SLC7A11 expression was measured to explore underlying mechanisms.
resultsMelanoma samples were divided into two subtypes with distinct tumor microenvironments. The eight-gene prognostic model accurately predicted patient outcomes in both training and validation cohorts. TMX4 was highly expressed in melanoma tissues, and its knockdown significantly inhibited the proliferation and migration of melanoma cells. Silencing of TMX4 enhanced oxidative stress by reducing GSH and increasing MDA and ROS, while upregulating SLC7A11 protein expression.
conclusionThe prognosis model based on DRGs has demonstrated potential predictive capability in melanoma. Functional experiments confirmed that TMX4 plays a role in regulating melanoma cell proliferation, migration, and redox homeostasis. These findings suggest that targeting TMX4 and its related pathways (potentially involving disulfidptosis) could be a promising therapeutic strategy for melanoma. However, further studies are required to validate its clinical applicability.
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.