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作 者:贾春丽[1] 路鹏霏 张华[1] JIA Chunli;LU Pengfei;ZHANG Hua(Cancer Center,the First Affiliated Hospital of Xinjiang Medical University,State Key Laboratory of Pathogenesis,Prevention and Treatment of High Incidence Diseases in Central Asia,Xinjiang Urumqi 830000,China)
机构地区:[1]省部共建中亚高发病成因与防治国家重点实验室,新疆医科大学第一附属医院肿瘤中心,新疆乌鲁木齐830000
出 处:《现代肿瘤医学》2024年第1期13-17,共5页Journal of Modern Oncology
基 金:省部共建国家重点实验室开放课题(编号:SKL-HIDCA-2020-31)。
摘 要:目的:研究GOLM1对人宫颈癌Siha细胞放射敏感性影响和可能机制。方法:构建慢病毒载体敲低宫颈癌细胞Siha中GOLM1的表达,qPCR检测干扰效率。采用4 Gy X线照射细胞后利用MTT实验检测细胞活性。将经射线照射后的宫颈癌细胞分为GOLM1-SiRNA组、NC-SiRNA组、GOLM1-SiRNA联合IGF1组,观察细胞形态,细胞侵袭和迁移实验观察侵袭和迁移能力,克隆形成实验检测细胞增殖能力。Western blot检测上皮间充质转化相关蛋白及PI3K/Akt通路蛋白。结果:经射线照射后,敲低Siha细胞中GOLM1表达组细胞活性下降最明显,细胞侵袭能力、迁移能力降低,克隆形成能力下降。GOLM1-SiRNA联合PI3K/Akt信号转导通路激活剂IGF1组细胞侵袭、迁移能力增加,克隆形成能力增强。降低GOLM1的表达增强了上皮标记蛋白E-cadherin的表达,同时降低了间质标记蛋白N-cadherin和p-Akt的表达,加入IGF1后E-cadherin蛋白的表达降低,N-cadherin和p-Akt蛋白的表达增强。结论:GOLM1表达降低增加了射线照射后宫颈癌细胞对放射线的敏感性。该作用可能通过介导PI3K/Akt信号转导通路影响细胞的侵袭及迁移能力实现的。Objective:To investigate the effect of GOLM1 on radiosensitivity of human cervical cancer Siha cells and its possible mechanism.Methods:A lentivirus vector was constructed to knock down the expression of GOLM1 in cervical cancer cell Siha,and the interference efficiency was detected by qPCR.Cells were irradiated with 4 Gy X-ray and their activity was detected using MTT assay.Cervical cancer cells irradiated with radiation were divided into GOLM1-SiRNA group,NC-SiRNA group,and GOLM1-SiRNA combined with IGF1 group.Cell morphology was observed,invasion and migration abilities were observed by cell invasion and migration experiments,and cell proliferation abilities were detected by clone formation experiments.Western blot was used to detect epithelial mesenchymal transformation related proteins and PI3K/Akt pathway proteins.Results:After irradiation,the cell activity of the knockdown group with GOLM1 expression in Siha cells decreased most significantly,and the invasive and migratory abilities of the cells decreased,as well as the clone formation ability decreased.The combination of GOLM1-SiRNA and PI3K/Akt signal transduction pathway activator IGF1 increased the ability of cell invasion and migration,and enhanced the ability of clone formation.Decreasing the expression of GOLM1 increased the expression of epithelial marker protein E-cadherin,while reducing the expression of interstitial marker proteins N-cadherin and p-Akt.After adding IGF1,the expression of E-cadherin protein decreased,while the expression of N-cadherin and p-Akt protein increased.Conclusion:The decreased expression of GOLM1 increases the sensitivity of cervical cancer cells to radiation after irradiation.This effect may be achieved by mediating the PI3K/Akt signal transduction pathway to affect the invasion and migration ability of cells.
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