ArticleGenes & genomics2025
OTOP3 functions as an oncogenic regulator of ferroptosis-mediated colorectal cancer progression.
Article in Genes & genomics, 2025. 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.
- Otopetrin 1 protects against adipose tissue wasting during cancer cachexia progression.iScience · 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
6 authors.
Funding
Abstract
backgroundOTOP3, a proton channel located at 17q25.1, drives colorectal cancer growth by enhancing c-Myc stability and inhibiting ferroptosis through GPX4 regulation. Inhibition of OTOP3 suppresses CRC proliferation via c-Myc destabilization, ROS accumulation, and lipid peroxidation, while modulating metabolic shifts linked to the Warburg effect. These findings position OTOP3 as a novel therapeutic target for CRC by disrupting oncogenic signaling and ferroptosis resistance.
objectiveTo investigate OTOP3's role in CRC growth/metastasis and its link to ferroptosis and metabolic reprogramming. To evaluate OTOP3 targeting as a therapeutic strategy.
methodsColorectal cancer (CRC) cell lines were transfected with OTOP3 siRNA to suppress gene expression, followed by cell viability assays to assess proliferation changes. Western blotting quantified c-Myc and GPX4 levels, while fluorescent probes measured ROS accumulation and lipid peroxidation. Ferroptosis induction was validated using ferroptosis inhibitors, and glycolytic activity was analyzed via glycolysis-related gene expression and lactate production assays.
resultsOTOP3 inhibition destabilized c-Myc, suppressed proliferation, and induced ferroptosis via GPX4 reduction, ROS accumulation, and lipid peroxidation. Altered glycolysis factors indicated enhanced Warburg effect.
conclusionOur study provides compelling evidence that targeting OTOP3 effectively suppresses colorectal cancer proliferation by reducing c-Myc protein stability and inducing ferroptosis. These effects are closely associated with metabolic shifts characteristic of the Warburg effect, emphasizing OTOP3 as a potential therapeutic target in colorectal cancer treatment.
Indexed as
Identifiers
40586985What 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.