首页|RRM2在骨肉瘤中的表达及其对骨肉瘤增殖的调控作用

RRM2在骨肉瘤中的表达及其对骨肉瘤增殖的调控作用

扫码查看
为了探究核糖核苷酸还原酶亚基M2(RRM2)在骨肉瘤中的作用,基于临床数据和基因表达谱交互分析数据库,分析RRM2在骨肉瘤中的表达模式及其预后价值.通过GEPIA和STRING数据库构建RRM2共表达网络,用免疫组化法证实RRM2与CDC27的相关性,对骨肉瘤细胞进行了集落形成和MTT实验,通过Western blot分析和qRT-qPCR验证RRM2对骨肉瘤的作用.进一步应用裸鼠皮下成瘤实验评价RRM2在体内对骨肉瘤的影响.结果表明,通过GEPIA数据库分析,发现高RRM2表达与较差的总生存期和无病生存期相关.在共表达网络中,RRM2在骨肉瘤中的功能与CDC27高度一致.RRM2能显著提高骨肉瘤细胞的集落数量和增殖率.进一步研究发现,RRM2在体内能促进骨肉瘤的生长.综上所述,RRM2在骨肉瘤中过表达且可促进细胞增殖,因此,RRM2可以作为骨肉瘤预后、诊断和治疗的有希望的生物标志物.
Expression of RRM2 in Osteosarcoma and Its Regulatory Effect on Proliferation of Osteosarcoma Cells
In order to investigate the role of ribonucleotide reductase subunit M2(RRM2)in osteosarcoma,the expression pattern and prognostic value of RRM2 in osteosarcoma were analyzed based on clinical data and gene expression profile interactive analysis database.The co-expression network of RRM2 was constructed by GEPIA and STRING databases,and the correlation between RRM2 and CDC27 was confirmed by immu-nohistochemistry.Colony formation and MTT experiments were performed in osteosarcoma cells,and the effect of RRM2 on osteosarcoma was verified by Western blot analysis and qRT-qPCR.The effect of RRM2 on osteosarcoma in vivo was further evaluated by subcutaneous tumor formation in nude mice.The results showed below:High RRM2 expression was associated with poor overall survival and disease-free survival through GEPIA database analysis.In the co-expression network,the function of RRM2 in osteosarcoma was highly consistent with that of CDC27.RRM2 could significantly increase the number and proliferation rate of os-teosarcoma cells.Further,RRM2 could promotes the growth of osteosarcoma in vivo.To sum up,RRM2 was overexpressed in osteosarcoma and could promote cell proliferation,and RRM2 could be used as a promising biomarker for the prognosis,diagnosis and treatment of osteosarcoma.

osteosarcomaRRM2proliferationGEPIA

李德尚、孙慧杰

展开 >

邢台市人民医院检验科,河北邢台 054000

邢台医学院医学技术系,河北邢台 054000

骨肉瘤 RRM2 增殖 GEPIA

2024

南开大学学报(自然科学版)
南开大学

南开大学学报(自然科学版)

CSTPCD北大核心
影响因子:0.284
ISSN:0465-7942
年,卷(期):2024.57(4)