热休克蛋白60（HSP60）对于新进入线粒体的蛋白质的折叠和组装至关重要。大多数类型的癌症都过度表达HSP60，但它与卵巢癌的关系仍在争议中。在比较正常人卵巢上皮细胞系和四种卵巢癌细胞系线粒体HSP60的表达水平后，选择SKOV3和OVCAR3作为实验模型。低的HSPD1（热休克蛋白家族D（HSP60）成员1）表达与卵巢癌患者不良预后有关。HSPD1的减少明显促进了卵巢癌细胞的增殖和迁移。在HSPD1敲除后不同表达的蛋白质在脂肪酸（LA）生物合成和代谢途径中富集，其中线粒体3-氧酰基ACP合成酶（OXSM）是最下调的蛋白质，负责脂肪酸合成。HSP60与OXSM相互作用并保持其稳定性。OXSM的过表达或LA处理可以逆转由HSPD1敲除介导的增殖促进。HSP60与OXSM相互作用。HSPD1的敲除可以通过降低OXSM和LA合成的蛋白质水平促进SKOV3和OVCAR3的增殖和迁移。 ©2023.作者（s）。

Heat shock protein 60 (HSP60) is essential for the folding and assembly of newly imported proteins to the mitochondria. HSP60 is overexpressed in most types of cancer, but its association with ovarian cancer is still in dispute. SKOV3 and OVCAR3 were used as experimental models after comparing the expression level of mitochondrial HSP60 in a normal human ovarian epithelial cell line and four ovarian cancer cell lines.Low HSPD1 (Heat Shock Protein Family D (HSP60) Member 1) expression was associated with unfavorable prognosis in ovarian cancer patients. Knockdown of HSPD1 significantly promoted the proliferation and migration of ovarian cancer cells. The differentially expressed proteins after HSPD1 knockdown were enriched in the lipoic acid (LA) biosynthesis and metabolism pathway, in which mitochondrial 3-oxoacyl-ACP synthase (OXSM) was the most downregulated protein and responsible for lipoic acid synthesis. HSP60 interacted with OXSM and overexpression of OXSM or LA treatment could reverse proliferation promotion mediated by HSPD1 knockdown.HSP60 interacted with OXSM and maintained its stability. Knockdown of HSPD1 could promote the proliferation and migration of SKOV3 and OVCAR3 via lowering the protein level of OXSM and LA synthesis.© 2023. The Author(s).