High MRPL12 expression drives esophageal cancer proliferation, invasion and migration

Mitochondrial dysfunction and metabolic reprogramming contribute to the occurrence and progression of esophageal squamous cell carcinoma (ESCC). Several studies confirmed the involvement of mitochondrial ribosomal protein L12 (MRPL12) in regulating mitochondrial metabolism. Mitochondrial ribosomal protein L7/L12 (MRPL12) is a gene that regulates mitochondrial transcription. However, its role in esophageal tumorigenesis remains unknown.

MRPL12 expression in ESCC and its transcription factors were assessed by Online databases. Its expression in ESCC tissues from oesophageal cancer patients, patient-derived ESCC tissues, and cell lines was detected by western blotting, RT-qPCR and immunohistochemistry. A series of cellular experiments, including gene knockout and overexpression were performed in esophageal cancer cell lines. Scratch assay, Transwell assay and CCK-8 cell viability assay were performed to establish the proliferation and migration of esophageal cancer cell lines.

A significant MRPL12 upregulation was observed in ESCC cells and tissues. MRPL12 overexpression promoted cell proliferation, migration, and invasion in vitro, while MRPL12 knockout induced the opposite effect. Subsequently, the most relevant transcription factors ZNF460 and ZNF135 for MRPL12 were found by online databases.

A new role of MRPL12 in ESCC was discovered. MRPL12 represented a potential prognostic biomarker for ESCC, and the reduction in MRPL12 expression might be a potential therapeutic approach to inhibit ESCC progression.