# MRS2 and mitochondrial gene networks in endometrial cancer: mechanisms, biomarkers, and therapeutic implications

## TL;DR

This study explores how the MRS2 protein and mitochondrial gene networks contribute to endometrial cancer progression and identifies MRS2 as a potential therapeutic target.

## Contribution

The study reveals a novel functional role of MRS2 in endometrial cancer progression through mitochondrial mechanisms.

## Key findings

- Elevated lactate levels correlate with increased MRS2 expression in endometrial cancer cells.
- MRS2 knockdown reduces cell proliferation, suggesting its role in cancer progression.
- MRS2 is linked to increased ROS production and altered mitochondrial gene expression.

## 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.