ArticlePeerJ2026
MRS2 and mitochondrial gene networks in endometrial cancer: mechanisms, biomarkers, and therapeutic implications.
Article in PeerJ, 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
13 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Magnesium ions and their transport proteins are increasingly recognized for their critical roles in tumor progression. However, their specific mechanisms in endometrial cancer (EC) remain poorly understood. This study investigated the role of Mitochondrial RNA Splicing 2 protein (MRS2), a key mitochondrial magnesium transporter, and its associated genes, in regulating mitochondrial function and the invasive and metastatic capabilities of EC cells. Using a combination of experimental approaches including lactate detection, flow cytometry, immunofluorescence, CCK8 assays, and Transwell migration assays, along with bioinformatics analysis, we investigated the relationship between lactate levels and MRS2 expression in endometrial cancer cells (KLE). Our findings suggest that elevated lactate levels are associated with increased MRS2 expression in mitochondria. This correlation was further linked to enhanced reactive oxygen species (ROS) production and altered expression of mitochondrial-related genes. Notably, MRS2 knockdown resulted in reduced proliferation of KLE cells, supporting a potential functional role of MRS2 in endometrial cancer progression. These findings provide new insights into the molecular mechanisms underlying EC progression and highlight MRS2 as a potential therapeutic target.
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.