The tumor-promoting role of methionyl-tRNA synthetase 1 in ovarian cancer and its potential mechanisms
Methionyl-tRNA synthetase 1 (MARS) is an enzyme that belongs to the family of aminoacyl-tRNA synthetases. High levels of MARS have been shown to correlate with a poorer prognosis in a variety of tumor types. However, its specific role and the underlying mechanism in cancer, especially in ovarian cancer, are not well understood. This study aims to investigate the roles and potential mechanisms of MARS in ovarian cancer. Our findings reveal that MARS protein levels are elevated in ovarian cancer tissues, and that high MARS expression is associated with reduced overall survival and progression-free survival. Silencing of MARS significantly inhibited the proliferation, colony formation, migration, and invasion of ovarian cancer cells in vitro and mildly suppressed ovarian tumor growth in vivo. MARS silencing contributes to the upregulation of p53 protein. Moreover, RNA sequencing and subsequent in vitro and in vivo validation showed that the TP53-regulated cell cycle genes and immune-related cell surface receptor and cytokine-encoding genes were downregulated following MARS knockdown, suggesting a potential mechanism for the observed attenuation of tumor progression. Our results suggest MARS as a potential biomarker and therapeutic target in ovarian cancer, highlighting the need for further investigation into its multifaceted role in tumor biology and immune cell function.