Origin recognition complex subunit 1(ORC1) is reported to be closely associated with the cell cycle. However, studies on the role of ORC1 in glioma remain undefined. The aim of the present study was to determine whether ORC1 affects cell migration, invasion, apoptosis, and proliferation and to explore the possible underlying mechanism. GEO database analysis indicated that ORC1 was significantly upregulated in glioma, while Gene set enrichment analysis (GSEA) analysis indicated that ORC1 primarily regulated the cell cycle and affects apoptotic signaling pathways. Analysis of protein-protein interaction (PPI) and gene ontology (GO) to further study the relevant mechanisms revealed that the function of the interaction between proteins and ORC1 was primarily concentrated in the regulation of cell cycle, and apoptosis played a critical role in the whole PPI network. Western blot assay and RT-PCR assay indicated that ORC1 was significantly upregulated in glioma tissues. Western blot assay and RT-PCR indicated that ORC1 was significantly upregulated in glioma cell lines. Cell migration, invasion, apoptosis, and proliferation were detected using Transwell and wound healing assays, flow cytometry, colony formation, and CCK8, respectively. Furthermore, OCR1 inhibition reduced invasion and migration, promoted cell apoptosis. In addition, OCR1 overexpression promoted cell proliferation and induced G2 phase arrest. Moreover, OCR1 downregulation suppressed activation of the ERK/JNK signaling pathway. The effects of ORC1 on biological processes were reversed by ERK and JNK inhibitors. These results indicate that ORC1 could be a novel prognostic marker of glioma via the activation of the ERK/JNK signaling pathway.

中文翻译：

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起源识别复合物亚基1通过改变ERK和JNK信号通路的激活来调节神经胶质瘤细胞的生长和转移。

据报道，起源识别复合物亚基1（ORC1）与细胞周期密切相关。然而，关于ORC1在神经胶质瘤中的作用的研究仍未确定。本研究的目的是确定ORC1是否影响细胞迁移，侵袭，凋亡和增殖，并探讨可能的潜在机制。GEO数据库分析表明，ORC1在神经胶质瘤中显着上调，而基因集富集分析（GSEA）分析表明，ORC1主要调节细胞周期并影响凋亡信号通路。对蛋白质间相互作用（PPI）和基因本体论（GO）进行分析以进一步研究相关机制后发现，蛋白质与ORC1之间的相互作用主要集中在细胞周期的调控中，细胞凋亡在整个PPI网络中起着至关重要的作用。Western blot法和RT-PCR法检测表明ORC1在神经胶质瘤组织中显着上调。蛋白质印迹分析和RT-PCR表明，ORC1在神经胶质瘤细胞系中显着上调。分别使用Transwell和伤口愈合测定，流式细胞仪，集落形成和CCK8检测细胞迁移，侵袭，凋亡和增殖。此外，OCR1抑制可减少侵袭和迁移，促进细胞凋亡。此外，OCR1过表达促进细胞增殖并诱导G2期阻滞。此外，OCR1下调抑制了ERK / JNK信号通路的激活。ORC1对生物过程的影响被ERK和JNK抑制剂逆转。