Song Wei, Yuan Yuan, Cao Fangfang, Pan Huazheng, Liu Yaqing
Department of Clinical Laboratory, The Affiliated Hospital of Qingdao University, Qingdao 266000, P. R. China.
J Microbiol. 2025 Apr;63(4):e2411018. doi: 10.71150/jm.2411018. Epub 2025 Apr 29.
The poor prognosis and high recurrence rate of ovarian cancer highlight the urgent need to develop new therapeutic strategies. Oncolytic Newcastle disease virus (NDV) can kill cancer cells directly and regulate innate and adaptive immunity. In this study, ovarian cancer cells infected with or without velogenic NDV-BJ were subjected to a CCK-8 assay for detecting cell proliferation, flow cytometry for detecting the cell cycle and apoptosis, and wound healing and transwell assays for detecting cell migration and invasion. Transcriptomic sequencing was conducted to identify the differentially expressed genes (DEGs). GO and KEGG enrichment analyses were performed to explore the mechanism underlying the oncolytic effect of NDV on ovarian cancer cells. The results showed that infection with NDV inhibited ovarian cancer cell proliferation, migration, and invasion; disrupted the cell cycle; and promoted apoptosis. Compared with those in negative control cells, the numbers of upregulated and downregulated genes in ovarian cancer cells infected with NDV were 1,499 and 2,260, respectively. Thirteen KEGG pathways related to cell growth and death, cell mobility, and signal transduction were significantly enriched. Among these pathways, 48 DEGs, especially SESN2, HLA B/C/E, GADD45B, and RELA, that may be involved in the oncolytic process were screened, and qPCR analysis verified the reliability of the transcription data. This study discovered some key pathways and genes related to oncolytic NDV-induced phenotypic changes in ovarian cancer cells, which will guide our future research directions and help further explore the specific mechanisms by which infection with NDV suppresses ovarian cancer development.
卵巢癌的不良预后和高复发率凸显了开发新治疗策略的迫切需求。溶瘤新城疫病毒（NDV）可直接杀死癌细胞并调节先天性和适应性免疫。在本研究中，对感染或未感染强毒株NDV-BJ的卵巢癌细胞进行CCK-8检测以检测细胞增殖，进行流式细胞术检测细胞周期和凋亡，进行伤口愈合和Transwell检测以检测细胞迁移和侵袭。进行转录组测序以鉴定差异表达基因（DEG）。进行GO和KEGG富集分析以探索NDV对卵巢癌细胞溶瘤作用的潜在机制。结果表明，感染NDV可抑制卵巢癌细胞的增殖、迁移和侵袭；扰乱细胞周期；并促进细胞凋亡。与阴性对照细胞相比，感染NDV的卵巢癌细胞中上调和下调基因的数量分别为1499个和2260个。13条与细胞生长和死亡、细胞迁移及信号转导相关的KEGG通路显著富集。在这些通路中，筛选出48个可能参与溶瘤过程的DEG，尤其是SESN2、HLA B/C/E、GADD45B和RELA，qPCR分析验证了转录数据的可靠性。本研究发现了一些与溶瘤性NDV诱导卵巢癌细胞表型变化相关的关键通路和基因，这将为我们未来的研究方向提供指导，并有助于进一步探索感染NDV抑制卵巢癌发展的具体机制。
