# Cytochrome c Oxidase Subunit 5A (COX5A) Enhances Gastric Cancer Progression by Augmenting ATP Synthesis and Activating the PI3K/Akt Pathway

## TL;DR

This study shows that COX5A promotes gastric cancer by boosting energy production and activating a key signaling pathway, making it a potential target for treatment.

## Contribution

COX5A is identified as a novel metabolic driver and therapeutic target in gastric cancer through its role in ATP synthesis and PI3K/Akt activation.

## Key findings

- COX5A upregulation correlates with poor survival in gastric cancer patients.
- COX5A enhances ATP production and activates the PI3K/Akt pathway to promote cancer progression.
- COX5A silencing reduces tumor growth in xenograft models.

## Abstract

Gastric cancer (GC) is a lethal malignancy characterised by poor prognosis. In this study, we identify cytochrome c oxidase subunit 5A (COX5A) as a key metabolic driver and prognostic biomarker in GC. COX5A was upregulated in tumours and correlated with poor survival. Mechanistically, COX5A enhanced mitochondrial oxidative phosphorylation to elevate ATP production, activating PI3K/Akt signalling to drive proliferation, migration, and invasion. These effects were reversed by PI3K/Akt inhibitors. JC‐1 assays revealed COX5A‐mediated mitochondrial membrane potential elevation, indicating amplified bioenergetic output. In vivo, COX5A silencing suppressed xenograft tumour growth. Our results demonstrate COX5A orchestrates metabolic reprogramming and PI3K/Akt‐mediated progression in GC, positioning it as both a prognostic indicator and therapeutic target.