上调NOL7表达通过诱导EMT进程抑制卵巢高级别浆液性癌侵袭转移并改善预后

Upregulation of NOL7 Expression Inhibits Invasion and Metastasis in High-Grade Serous Ovarian Carcinoma by Suppressing the EMT Process and Improving Prognosis

摘要: 目的：探讨核蛋白NOL7在卵巢高级别浆液性癌(HGSC)中的表达特征及其对肿瘤恶性行为的调控机制。方法：回顾性分析120例HGSC患者临床资料，免疫组化检测NOL7表达并分析其与临床病理参数、预后的相关性；构建慢病毒过表达NOL7细胞模型，通过CCK-8增殖实验、划痕/Transwell迁移侵袭实验、Western Blot检测EMT相关蛋白表达。结果：临床分析显示NOL7低表达率高达73.3% (88/120)，与肿瘤长径 > 8 cm (χ² = 20.89)、晚期FIGO分期(III~IV期，χ² = 15.76)、低分化(χ² = 32.18)及淋巴结转移(χ² = 26.34)显著相关(均P < 0.05)，且低表达组10个月生存率显著降低至0.80 (95%CI: 0.75~0.85) vs高表达组0.90 (log-rank χ² = 24.76, P < 0.001)。体外实验证实NOL7过表达可抑制细胞增殖(72 h抑制率29.2%)、迁移(迁移率降至21.54% ± 3.49%)及侵袭(穿膜细胞减少75.2%)，并上调E-cadherin (0.82 ± 0.07 vs 0.47 ± 0.05)、下调Vimentin (0.28 ± 0.03 vs 0.78 ± 0.07)等EMT标志物(均P < 0.05)。结论：NOL7作为抑癌分子可能通过阻断EMT进程抑制HGSC进展，其表达水平具有预后评估价值(AUC = 0.86)。

Abstract: Objective: To investigate the expression characteristics of nuclear protein NOL7 in high-grade serous ovarian carcinoma (HGSC) and its regulatory mechanism on malignant tumor behavior. Methods: Clinical data from 120 HGSC patients were retrospectively analyzed. Immunohistochemical (IHC) analysis was performed to detect NOL7 expression and its correlation with clinicopathological parameters and prognosis. Lentivirus-mediated NOL7 overexpression cell models were established. Cell proliferation was assessed using CCK-8 assays, migration and invasion abilities were evaluated by scratch wound healing and Transwell assays, and epithelial-mesenchymal transition (EMT)-related proteins were detected via Western blotting. Results: Clinical analysis revealed a low NOL7 expression rate of 73.3% (88/120), significantly associated with tumor size > 8 cm (χ² = 20.89), advanced FIGO stage (III~IV, χ² = 15.76), poor differentiation (χ² = 32.18), and lymph node metastasis (χ² = 26.34) (all P < 0.05). The 10-month survival rate in the low-expression group was significantly reduced to 0.80 (95%CI: 0.75~0.85) versus 0.90 in the high-expression group (log-rank χ² = 24.76, P < 0.001). In vitro experiments confirmed that NOL7 overexpression inhibited cell proliferation (inhibition rate: 29.2% at 72 h), migration (migration rate decreased to 21.54% ± 3.49%), and invasion (transmembrane cell count reduced by 75.2%). Furthermore, it upregulated EMT markers such as E-cadherin (0.82 ± 0.07 vs 0.47 ± 0.05) and downregulated Vimentin (0.28 ± 0.03 vs 0.78 ± 0.07) (all P < 0.05). Conclusion: NOL7 may act as a tumor suppressor by inhibiting HGSC progression through blocking the EMT process, and its expression level holds prognostic value (AUC = 0.86).