卵巢癌（OC）是一种妇科恶性肿瘤，是全球最常见的女性癌症之一，显着降低患者的生活质量。线粒体载体同源 2 (MTCH2) 是一种线粒体外膜蛋白，在线粒体代谢和细胞死亡中发挥调节作用。 MTCH2 在 OC 发展背景下的确切贡献和潜在分子途径目前尚不清楚。本研究旨在探讨MTCH2在OC细胞能量代谢、细胞增殖和转移潜能中的作用，并评估MTCH2、氨酰转移RNA合成酶相互作用多功能蛋白2（AIMP2）和claudin-3之间的调节关系。对 67 名高级浆液性 OC 患者的分析表明，与 OC 组织样本附近的相应正常组织相比，OC 肿瘤组织样本中 MTCH2、AIMP2 和 Claudin-3 的表达水平升高。 MTCH2 过表达与 OC 肿瘤样本的国际妇产科联合会分期和肿瘤分化显着相关。使用SK-OV-3 OC细胞系的体外实验表明，MTCH2对这些细胞的细胞增殖、侵袭和迁移能力发挥调节作用。敲除 MTCH2 会减少 SK-OV-3 OC 细胞中 ATP 的产生，诱导线粒体功能障碍并促进细胞骨架重塑和凋亡。此外，MTCH2 敲除下调了claudin-3 和AIMP2 蛋白的表达水平。 AIMP2 的敲低抑制了 MTCH2 的调节作用。免疫共沉淀实验表明 MTCH2 与 AIMP2 和claudin-3 相互作用。本研究为卵巢癌转移的治疗提供了新的见解，因为MTCH2被证明通过AIMP2调节claudin-3在OC细胞的进展中发挥作用，这可以为卵巢癌转移的治疗提供新的见解。 ：© 2024 Sun 等人。

Ovarian cancer (OC) is a gynecological malignancy that ranks among the most common female cancers worldwide and notably reduces a patient's quality of life. Mitochondrial carrier homology 2 (MTCH2) is a mitochondrial outer membrane protein that serves a regulatory role in mitochondrial metabolism and cell death. The precise contribution and underlying molecular pathways of MTCH2 in the context of OC development is currently unclear. The present study aimed to investigate the roles of MTCH2 in the energy metabolism, cell proliferation and metastatic potential of OC cells and evaluate the regulatory relationship between MTCH2, aminoacyl transfer RNA synthetase-interacting multifunctional protein 2 (AIMP2) and claudin-3. An analysis of 67 patients with high-grade serous OC demonstrated increased expression levels of MTCH2, AIMP2 and claudin-3 in OC tumor tissue samples compared with in corresponding normal tissues adjacent to OC tissue samples. MTCH2 overexpression was significantly associated with the International Federation of Gynecology and Obstetrics stage and tumor differentiation of the OC tumor samples. In vitro experiments using the SK-OV-3 OC cell line demonstrated that MTCH2 exerts a regulatory effect on the cell proliferation, invasion and migratory capabilities of these cells. Knockdown of MTCH2 reduced ATP production, induced mitochondrial dysfunction and promoted cytoskeleton remodeling and apoptosis in SK-OV-3 OC cells. In addition, MTCH2 knockdown downregulated the expression levels of both claudin-3 and AIMP2 proteins. Knockdown of AIMP2 inhibited the regulatory effect of MTCH2. Co-immunoprecipitation experiments demonstrated that MTCH2 interacts with AIMP2 and claudin-3. The present study provides novel insights into the treatment of OC metastasis, as MTCH2 was demonstrated to serve roles in the progression of OC cells through the regulation of claudin-3 via AIMP2, which could provide novel insights into the treatment of ovarian cancer metastasis.Copyright: © 2024 Sun et al.