您的位置:山东大学 -> 科技期刊社 -> 《山东大学学报(医学版)》

山东大学学报 (医学版) ›› 2018, Vol. 56 ›› Issue (2): 9-13.doi: 10.6040/j.issn.1671-7554.0.2017.952

• 基础医学 • 上一篇    下一篇

干扰PRPS2基因表达对宫颈癌细胞生物学特性的影响

陈颖,周小青,齐眉,张魏芳,刘娟,赵蔚明   

  1. 山东大学齐鲁医学院基础医学院病原生物学系, 山东 济南 250012
  • 发布日期:2022-09-28
  • 通讯作者: 赵蔚明. E-mail:zhaowm@sdu.edu.cn刘娟. E-mail:liujuan@sdu.edu.cn
  • 基金资助:
    国家自然科学基金(81472552);山东省自然科学基金(ZR2017MH092)

Effects of PRPS2 knockdown on the biological property of cervical cancer cells

CHEN Ying, ZHOU Xiaoqing, QI Mei, ZHANG Weifang, LIU Juan, ZHAO Weiming   

  1. Department of Pathogenic Biology, School of Basic Medical Sciences, Cheeloo College of Medical, Shandong University, Jinan 250012, Shandong, China
  • Published:2022-09-28

摘要: 目的 探讨磷酸核糖焦磷酸合成酶2(PRPS2)对宫颈癌细胞HeLa生长增殖、迁移侵袭以及细胞周期和凋亡的影响。 方法 采用Western blotting法检测宫颈癌细胞HeLa和正常表皮细胞中PRPS2蛋白的基础表达。应用Lipofectamine 2000将PRPS2特异性小干扰RNA(siPRPS2)转染至人宫颈腺癌细胞(HeLa)中,并设置相应对照组,采用Western blotting法检测PRPS2的干扰效率;采用Cell Counting Kit8细胞增殖试剂盒(CCK-8)、细胞克隆实验和Transwell侵袭实验检测细胞生长增殖、迁移和侵袭能力;采用流式细胞术检测PRPS2对细胞周期和凋亡的影响。 结果 PRPS2在HeLa细胞中呈高表达,siPRPS2可有效抑制HeLa细胞PRPS2蛋白的表达(抑制率为70%);CCK-8和克隆实验显示干扰PRPS2表达后,HeLa细胞的活性和增殖能力明显下降(P<0.001, P<0.01);Transwell实验表明,敲低PRPS2后,HeLa细胞迁移和侵袭至下室的细胞数明显减少(P<0.05, P<0.001);敲低PRPS2后HeLa细胞周期发生G2阻滞(P<0.001),并且细胞凋亡比例升高(P=0.012)。 结论 PRPS2可促进宫颈癌细胞的生长增殖、侵袭转移和推动细胞周期进程。

关键词: 宫颈癌, 磷酸核糖焦磷酸合成酶2, 增殖, 迁移, 侵袭

Abstract: Objective To evaluate the role of phosphoribosyl-pyrophosphate synthetase 2(PRPS2)on the proliferation, metastasis, cell cycle and cell apoptosis of cervical cancer cells. Methods The basal expressions of PRPS2 in cervical cancer cells(HeLa cells)and normal epithelial cells were detected with Western blotting. HeLa cells were transfected with PRPS2-specific siRNA(siPRPS2)via Lipofectamine 2000, and then divided into the knockdown group and control group. The knockdown efficiency of PRPS2 was determined with Western blotting. The cell proliferation, migration and invasion were detected with CCK-8, colony formation and Transwell assays. The effect of PRPS2 on cell cycle and apoptosis were examined with flow cytometry. Results PRPS2 was highly expressed in HeLa cells, and siPRPS2 effectively inhibited the expression of PRPS2(inhibition ratio 70%). CCK-8 and colony formation assays indicated that PRPS2 knockdown significantly inhibited the viability(P<0.001)and proliferation(P<0.01)of HeLa cells. Transwell assays showed that PRPS2 knockdown obviously reduced the number of migrated(P<0.05)and invaded(P<0.001)cells through the membrane. PRPS2 knockdown contributed to G2/M arrest(P<0.001)and apoptosis of cervical cancer cells(P=0.012). Conclusion PRPS2 can promote the proliferation, metastasis and cell cycle of cervical cancer cells.

Key words: Cervical cancer, Phosphoribosyl-pyrophosphate synthetase 2, Proliferation, Migration, Invasion

中图分类号: 

  • R737
[1] Hove-Jensen B, Andersen KR, Kilstrup M, et al. Phosphoribosyl diphosphate(PRPP): biosynthesis, enzymology, utilization, and metabolic significance[J]. MicrobiolMolBiol Rev, 2016, 81(1). pii: e00040-16. doi: 10.1128/MMBR.00040-16.
[2] de Brouwer AP, van Bokhoven H, Nabuurs SB, et al. PRPS1 mutations: four distinct syndromes and potential treatment[J]. Am J Hum Genet, 2010, 86(4): 506-518.
[3] Iizasa T. Increased activity of PRPP synthetase[J]. Nihon Rinsho, 2008, 66(4): 694-698.
[4] Cunningham JT, Moreno MV, Lodi A, et al. Protein and nucleotide biosynthesis are coupled by a single rate-limiting enzyme, PRPS2, to drive cancer[J]. Cell, 2014, 157(5): 1088-1103.
[5] Schiffman M, Doorbar J, Wentzensen N, et al. Carcinogenic human papillomavirus infection[J]. Nature reviews Disease primers, 2016, 2(1): 16086.
[6] Münger K, Baldwin A, Edwards KM, et al. Mechanisms of human papillomavirus induced oncogenesis[J]. J Virol, 2004, 78(21): 11451-11460.
[7] Zhang X, Chen H, Wang X, et al. Expression and transcriptional profiling of the LKB1 tumor suppressor in cervical cancer cells[J]. GynecolOncol, 2014, 134(2): 372-378.
[8] Cairns RA, Harris IS, Mak TW. Regulation of cancer cell metabolism[J]. Nat Rev Cancer, 2011, 11(2): 85-95.
[9] Mayers JR, Vander Heiden MG. Nature and nurture: what determines tumor metabolic phenotypes?[J]. Cancer Res, 2017, 77(12): 3131-3134.
[10] Martinez-Outschoorn UE, Peiris-Pages M, Pestell RG, et al. Cancer metabolism: A therapeutic perspective[J]. Nat Rev Clin Oncol, 2016, 14(2): 11-31.
[11] Xue C, Yu DM, Gherardi S, et al. MYCN promotes neuroblastoma malignancy by establishing aregulatory circuit with transcription factor AP4[J]. Oncotarget, 2016, 7(34): 54937-54951.
[12] Lei B, Wan B, Peng J, et al. PRPS2 expression correlates with sertoli-cell only syndrome and inhibits the apoptosis of TM4 sertoli cells[J]. J Urol, 2015, 194(5): 1491-1497.
[13] Mannava S, Grachtchouk V, Wheeler LJ, et al. Direct role of nucleotide metabolism in C-MYC-dependent proliferation of melanoma cells[J]. Cell Cycle, 2008, 7(15): 2392-2400.
[14] Wang J, Wang J, Zhang Y, et al. Proteomic analysis on infantile spasm and prenatal stress[J]. Epilepsy Res, 2014, 108(7): 1174-1183.
[15] zur Hausen H. Papillomaviruses and cancer: from basic studies to clinical application[J]. Nat Rev Cancer, 2002, 2(5): 342-350.
[16] zur Hausen H. Papillomaviruses in the causation of human cancers -a brief historical account[J]. Virology, 2009, 384(2): 260-265.
[1] 王晓磊 张海涛 张辉 郭成浩. 舒血宁注射液对高碘致培养血管内皮细胞损伤的保护作用[J]. 山东大学学报(医学版), 2209, 47(6): 38-.
[2] 殷悦,莫振飞,吴培昕,刘金霞,魏元辉,任佳博,李春笋. GPX1基因在肺癌中的表达特征及其对肺腺癌细胞增殖、迁移、侵袭、凋亡的影响[J]. 山东大学学报 (医学版), 2026, 64(1): 65-73.
[3] 韩觉明,王晖,吴倩,郑慧玲,朱琳. B4GALNT4促进肺腺癌细胞增殖、迁移和侵袭能力[J]. 山东大学学报 (医学版), 2025, 63(7): 23-31.
[4] 王磊,常霄,王梓萌,李娇娇,崔书君,杨飞,朱月香. 瘤内及瘤周DCE-MRI影像组学对宫颈癌患者无进展生存期的预测价值[J]. 山东大学学报 (医学版), 2025, 63(6): 45-54.
[5] 李观强,施昱诚,朱可涵,胡波,黄献琛,孙元,李笃信,张喜成. 蜗牛粘液来源的活性肽SK-14促进成纤维细胞的增殖和迁移[J]. 山东大学学报 (医学版), 2025, 63(11): 1-7.
[6] 刘振昆,吕纪玲,徐伟伟,马力天,张才擎. BALF tNGS检测及培养对NSCLC合并IPFD的诊断价值[J]. 山东大学学报 (医学版), 2025, 63(11): 36-45.
[7] 张洁,张芳芳,王靖楠,李泽宇,宋颖,李娜. circ_0000144在乳腺癌中的表达及其对乳腺癌细胞增殖、迁移和侵袭能力的影响[J]. 山东大学学报 (医学版), 2025, 63(1): 35-42.
[8] 张学宇,张学海,孙文青,刘晗,姜金波,刘寒,李远,陈晓梅. 重症新型冠状病毒肺炎伴侵袭性肺曲霉病及反复致命性消化道出血1例[J]. 山东大学学报 (医学版), 2024, 62(7): 56-61.
[9] 曹华琳,贾彦召,曲莉,尹昕. CircFAT1调节miR-296-3p/MAPRE1轴对鼻咽癌细胞增殖、凋亡和放疗敏感性的影响[J]. 山东大学学报 (医学版), 2023, 61(9): 38-46.
[10] 金珊,高杰,谢玉姣,展垚,杜甜甜,王传新. 甲基转移酶PRMT5稳定USP15促进乳腺癌发生发展的作用[J]. 山东大学学报 (医学版), 2023, 61(7): 1-11.
[11] 任慧欣,郑茂金,韩文灿,王超群,周云,裴冬生. 过氧化氢通过调控自噬增强宫颈癌的放疗敏感性[J]. 山东大学学报 (医学版), 2023, 61(6): 22-28.
[12] 何静,严如根,武志红,李长忠. 消癥抑癌方对卵巢癌SKOV3细胞增殖、迁移的影响[J]. 山东大学学报 (医学版), 2023, 61(5): 1-10.
[13] 刘萌,侯丛哲,麻焕玉,张震,赵新蕊,张萍,朱琳. β-雌二醇对宫颈癌Hela细胞增殖的影响[J]. 山东大学学报 (医学版), 2023, 61(2): 9-15.
[14] 董相君,李娟,孔雪,李培龙,赵文静,梁怡然,王丽丽,杜鲁涛,王传新. 环状RNA hsa_circ_0008591对乳腺癌细胞生物学行为的影响[J]. 山东大学学报 (医学版), 2023, 61(2): 78-87.
[15] 赵舸,邹存华,宋冬冬,赵淑萍. 丹参酮IIA对子宫内膜癌细胞增殖与凋亡的影响[J]. 山东大学学报 (医学版), 2022, 60(9): 53-58.
Viewed
Full text


Abstract

Cited

  Shared   
  Discussed   
No Suggested Reading articles found!