ArticleBiochemistry and biophysics reports2026
The FOXM1-SESN2 axis maintains redox homeostasis and protects esophageal squamous carcinoma cells from oxidative stress.
Article in Biochemistry and biophysics reports, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
This study aimed to elucidate the role of ROS-related genes in esophageal squamous cell carcinoma (ESCC) prognosis and the cellular mechanisms involving FOXM1 and SESN2. A prognostic model incorporating six genes (FOXM1, SESN2, APOD, GATM, HEBP2, STAT1) was developed using three ESCC gene expression datasets via univariate Cox regression, LASSO-Cox algorithm, and multivariate validation. Functional assays revealed that FOXM1 knockdown elevated intracellular ROS and malondialdehyde (MDA) levels while reducing total glutathione and antioxidant capacity, impairing proliferation, migration, and cell cycle progression. RNA-seq and luciferase assays confirmed SESN2 as a transcriptional target of FOXM1. Dual knockdown of FOXM1 and SESN2 exacerbated oxidative stress, decreased mitochondrial membrane potential, and increased cell death, accompanied by mitochondrial morphological changes (reduced shrinkage, increased membrane density). Western blotting showed decreased BCL2 and GPX4 expression but increased LC3-II and
Indexed as
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.