Xu Shengjie, Qi Huizhi, Gong Weijian, Xu Juan, Jia Xuemei
Department of Gynecology, Nanjing Women and Children's Healthcare Hospital, Women's Hospital of Nanjing Medical University, Nanjing, 210004, PR China.
Nanjing Women and Children's Healthcare Institute, Nanjing Women and Children's Healthcare Hospital, Women's Hospital of Nanjing Medical University, Nanjing, 210004, PR China.
Med Oncol. 2025 Apr 29;42(6):187. doi: 10.1007/s12032-025-02741-1.
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.
甲硫氨酰 - tRNA合成酶1（MARS）是一种属于氨酰 - tRNA合成酶家族的酶。已表明高水平的MARS与多种肿瘤类型的较差预后相关。然而，其在癌症，尤其是卵巢癌中的具体作用和潜在机制尚不清楚。本研究旨在探讨MARS在卵巢癌中的作用和潜在机制。我们的研究结果显示，卵巢癌组织中MARS蛋白水平升高，且MARS高表达与总生存期和无进展生存期降低相关。MARS沉默在体外显著抑制卵巢癌细胞的增殖、集落形成、迁移和侵袭，并在体内轻度抑制卵巢肿瘤生长。MARS沉默导致p53蛋白上调。此外，RNA测序以及随后的体外和体内验证表明，MARS敲低后，TP53调控的细胞周期基因以及免疫相关细胞表面受体和细胞因子编码基因下调，这提示了观察到的肿瘤进展减弱的潜在机制。我们的结果表明MARS是卵巢癌的潜在生物标志物和治疗靶点，凸显了进一步研究其在肿瘤生物学和免疫细胞功能中的多方面作用的必要性。
