MRPL52 (mitochondrial ribosomal protein L52) is a nuclear-encoded mitochondrial protein that functions as a structural component of the mitochondrial large ribosomal subunit, participating in mitochondrial protein translation 1. Beyond its primary translational role, MRPL52 has emerged as a critical regulator in cancer biology and stress response. In breast cancer, MRPL52 expression is upregulated by hypoxia-inducible factor-1 (HIF-1) in response to hypoxic microenvironments 2. This upregulation promotes apoptotic resistance and metastatic initiation through dual mechanisms: suppression of mitochondrial apoptosis via PINK1/Parkin-dependent mitophagy to control reactive oxygen species (ROS) generation, and enhancement of epithelial-mesenchymal transition through ROS-Notch1-Snail signaling 2. In oral squamous cell carcinoma, MRPL52 transcription is activated by upstream transcription factor 1 (USF1), with long non-coding RNA LINC00152 enhancing this axis to promote tumor growth 3. Regarding ischemic injury, MRPL52 inhibition increased cell viability and attenuated oxygen-glucose deprivation/reperfusion-induced apoptosis 1. Additionally, MRPL52 was identified in a 19-gene signature predicting colorectal cancer survival 4 and in genetic variants associated with fibrotic disorders like adhesive capsulitis 5. These findings establish MRPL52 as a multifunctional protein linking mitochondrial bioenergetics to cancer progression and cellular stress responses.