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PSF1表达的敲低抑制体外肺癌细胞的增殖。

Knockdown of PSF1 expression inhibits cell proliferation in lung cancer cells in vitro.

作者信息

Zhang Jingyao, Wu Qifei, Wang Zhe, Zhang Yong, Zhang Guangjian, Fu Junke, Liu Chang

机构信息

Department of Hepatobiliary Surgery, the First Affiliated Hospital, Medical School, Xi'an Jiaotong University, Xi'an, China.

出版信息

Tumour Biol. 2015 Mar;36(3):2163-8. doi: 10.1007/s13277-014-2826-8. Epub 2014 Nov 15.

DOI:10.1007/s13277-014-2826-8
PMID:25398693
Abstract

Partner of sld five 1 (PSF1) is a member of the heterotetrameric complex termed GINS. Previous studies have shown that PSF1 is unregulated in several cancer and associated with tumor malignant characters. However, the effects of PSF1 in lung cancer are still unclear. The goal of this study was to investigate the effects of PSF1 on the proliferation capacities of lung cancer. To start with, expression of PSF1 in 22 human lung cancer samples and adjacent non-tumor samples were detected by real-time RT-PCR and Western blotting. Our results showed that PSF1 was overexpressed in lung cancer samples compared to adjacent non-tumor samples. To achieve better insights of PSF1 functions in lung cancer cells, we used PSF1-specific small interfering RNA (siRNA) successfully inhibit the expression of PSF1 in messenger RNA (mRNA) and protein levels. In addition, we used lung cancer cell lines with different p53 gene background (p53 null and p53 wild-type). The results showed that knockdown of PSF1 inhibited cell proliferation and caused cell cycle arrest of lung cancer cells in a p53-independent manner. Our data indicated that PSF1 is functionally involved in lung cancer cell proliferation and is a potential target for lung cancer therapy.

摘要

sld five 1的伴侣蛋白(PSF1)是名为GINS的异源四聚体复合物的成员。先前的研究表明,PSF1在多种癌症中表达失调,并与肿瘤恶性特征相关。然而,PSF1在肺癌中的作用仍不清楚。本研究的目的是探讨PSF1对肺癌增殖能力的影响。首先,通过实时逆转录-聚合酶链反应(RT-PCR)和蛋白质印迹法检测22例人肺癌样本及相邻非肿瘤样本中PSF1的表达。我们的结果显示,与相邻非肿瘤样本相比,PSF1在肺癌样本中过表达。为了更好地了解PSF1在肺癌细胞中的功能,我们使用PSF1特异性小干扰RNA(siRNA)成功抑制了PSF1在信使核糖核酸(mRNA)和蛋白质水平的表达。此外,我们使用了具有不同p53基因背景(p53缺失和p53野生型)的肺癌细胞系。结果表明,敲低PSF1可抑制肺癌细胞增殖,并以p53非依赖的方式导致肺癌细胞周期停滞。我们的数据表明,PSF1在功能上参与肺癌细胞增殖,是肺癌治疗的潜在靶点。

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本文引用的文献

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Drug repositioning discovery for early- and late-stage non-small-cell lung cancer.针对早期和晚期非小细胞肺癌的药物重新定位发现
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Int J Biol Markers. 2015 Feb 24;30(1):e56-64. doi: 10.5301/jbm.5000105.
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P53 induction accompanying G2/M arrest upon knockdown of tumor suppressor HIC1 in U87MG glioma cells.在U87MG胶质瘤细胞中,肿瘤抑制因子HIC1敲低后伴随G2/M期阻滞的P53诱导。
PAX5 和 circ1857 通过调节 GINS1 影响弥漫性大 B 细胞淋巴瘤的进展和 B 细胞增殖。
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DNA replication: Mechanisms and therapeutic interventions for diseases.DNA复制:疾病的机制与治疗干预措施
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6
Identification of GINS1 as a therapeutic target in the cancer patients infected with COVID-19: a bioinformatics and system biology approach.鉴定GINS1作为感染COVID-19的癌症患者的治疗靶点:一种生物信息学和系统生物学方法。
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Construction of a circular RNA-microRNA-messenger RNA regulatory network of hsa_circ_0043256 in lung cancer by integrated analysis.通过综合分析构建肺癌中 hsa_circ_0043256 的环状 RNA-微小 RNA-信使 RNA 调控网络。
Thorac Cancer. 2022 Jan;13(1):61-75. doi: 10.1111/1759-7714.14226. Epub 2021 Nov 21.
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Front Cell Dev Biol. 2021 Aug 3;9:711894. doi: 10.3389/fcell.2021.711894. eCollection 2021.
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Targeted therapies in development for non-small cell lung cancer.正在研发的非小细胞肺癌靶向疗法。
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