首页|RASA4表达失活促进鼻咽癌增殖的机制研究

RASA4表达失活促进鼻咽癌增殖的机制研究

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目的:探究RASA4基因在鼻咽癌(NPC)中的表达情况,研究RASA4基因对影响NPC增殖和转移的影响及分子机制.方法:利用GEO数据库进行NPC中RASA4转录水平的Meta分析.采用实时荧光定量PCR(RT-qPCR)和western blotting法检测NPC细胞中RASA4 mRNA及蛋白表达水平,免疫组织化学染色法检测RASA4在NPC组织中的蛋白表达及定位情况,CCK-8及平板克隆实验评估RASA4对NPC细胞增殖能力的影响.结果:基于GEO数据的生物信息学分析显示,RASA4在NPC中的mRNA表达显著下调.RT-qPCR和western blotting显示NPC细胞中RASA4 mRNA及蛋白表达下调.外源性过表达RASA4基因可抑制NPC细胞增殖.结论:RASA4可能是NPC潜在的抑制基因,研究其失活机制及其功能对于NPC的发生机制和治疗具有重要意义.
Mechanism of RASA4 expression inactivation promoting proliferation of nasopharyngeal car-cinoma
Objective:To explore the expression of RASA4gene in nasopharyngeal carcinoma(NPC),and to in-vestigate the influence and molecular mechanism of RASA4gene affecting the proliferation of NPC.Methods:Meta-analysis of RASA4transcription levels in NPC was performed using GEO database.RASA4mRNA and protein expression levels in NPC cell lines were detected by reverse transcription-quantitative PCR(RT-qPCR)and western blotting.RASA4protein expression and localization in NPC tissues were detected using immunohis-tochemistry(IHC).The impact of RASA4on cell proliferation was evaluated through cell counting kit-8(CCK-8)assay and colony formation assay.Results:Bioinformatics analysis based on GEO data showed that RASA4 mRNA expression was significantly down-regulated in NPC.RT-qPCR and western blotting results indicated that RASA4 was down-regulated at both mRNA and protein expression in NPC cells.Exogenous overexpression of the RASA4gene could inhibit the cell proliferation of NPC.Conclusion:RASA4may serve as a potential sup-pressor gene in NPC,and investigating its inactivation mechanism and function is of significant importance for the pathogenesis and treatment of NPC.

nasopharyngeal carcinomaRASA4cell proliferation

汤诗玥、赵军、张海山、李丽媚、周晓莹、黄议莹、温文胜

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广西医科大学第一附属医院耳鼻喉头颈外科,南宁 530021

广西医科大学区域性高发肿瘤早期防治研究教育部重点实验室,南宁 530021

广西区域性高发肿瘤早期防治研究重点实验室,南宁 530021

鼻咽癌 RASA4 细胞增殖

国家自然科学基金国家自然科学基金区域性高发肿瘤早期防治研究教育部重点实验室广西重点实验室自主课题

8186047981960490GKE-ZZ 202145

2024

广西医科大学学报
广西医科大学

广西医科大学学报

CSTPCD
影响因子:0.788
ISSN:1005-930X
年,卷(期):2024.41(4)
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