The key pathways and genes related to oncolytic Newcastle disease virus-induced phenotypic changes in ovarian cancer cells.

IF 3.3 4区 生物学 Q2 MICROBIOLOGY
Journal of Microbiology Pub Date : 2025-04-01 Epub Date: 2025-04-29 DOI:10.71150/jm.2411018
Wei Song, Yuan Yuan, Fangfang Cao, Huazheng Pan, Yaqing Liu
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引用次数: 0

Abstract

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.

溶瘤性新城疫病毒诱导卵巢癌细胞表型变化的关键途径和相关基因
卵巢癌预后差,复发率高,迫切需要开发新的治疗策略。溶瘤性新城疫病毒(NDV)可直接杀死癌细胞,并调节先天免疫和适应性免疫。在本研究中,对感染或未感染NDV-BJ的卵巢癌细胞进行CCK-8检测细胞增殖,流式细胞术检测细胞周期和凋亡,伤口愈合和transwell检测细胞迁移和侵袭。转录组测序鉴定差异表达基因(DEGs)。通过GO和KEGG富集分析,探讨NDV对卵巢癌细胞溶瘤作用的机制。结果表明,NDV感染可抑制卵巢癌细胞的增殖、迁移和侵袭;破坏细胞周期;促进细胞凋亡。与阴性对照细胞相比,NDV感染的卵巢癌细胞中上调和下调的基因数量分别为1499个和2260个。13条与细胞生长和死亡、细胞迁移和信号转导相关的KEGG通路显著富集。其中筛选到48个可能参与溶瘤过程的基因通路,特别是SESN2、HLA B/C/E、GADD45B、RELA, qPCR分析验证了转录数据的可靠性。本研究发现了溶瘤性NDV诱导卵巢癌细胞表型变化的一些关键通路和相关基因,这将指导我们未来的研究方向,并有助于进一步探索NDV感染抑制卵巢癌发展的具体机制。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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来源期刊
Journal of Microbiology
Journal of Microbiology 生物-微生物学
CiteScore
5.70
自引率
3.30%
发文量
0
审稿时长
3 months
期刊介绍: Publishes papers that deal with research on microorganisms, including archaea, bacteria, yeasts, fungi, microalgae, protozoa, and simple eukaryotic microorganisms. Topics considered for publication include Microbial Systematics, Evolutionary Microbiology, Microbial Ecology, Environmental Microbiology, Microbial Genetics, Genomics, Molecular Biology, Microbial Physiology, Biochemistry, Microbial Pathogenesis, Host-Microbe Interaction, Systems Microbiology, Synthetic Microbiology, Bioinformatics and Virology. Manuscripts dealing with simple identification of microorganism(s), cloning of a known gene and its expression in a microbial host, and clinical statistics will not be considered for publication by JM.
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