CYTOR通过调控miR-125b-5p/HK2通路促进宫颈癌细胞有氧糖酵解、增殖和侵袭

CYTOR promotes aerobic glycolysis, proliferation and invasion of cervical cancer cells by regulating miR-125b-5p/HK2 pathway

探讨细胞骨架RNA(CYTOR)及其下游分子轴对宫颈癌细胞增殖和侵袭的影响。选取宫颈癌组织及细胞,检测CYTOR的表达水平;采用CCK-8、Transwell、有氧糖酵解方法检测探讨CYTOR对宫颈癌细胞增殖、侵袭和有氧糖酵解的影响;同时利用双荧光素酶报告基因验证CYTOR、小分子RNAmiR-125b-5p、己糖激酶2(HK2)之间的相互作用关系。结果显示,CYTOR在宫颈癌组织及细胞中明显上调(P<0.05);抑制CYTOR可明显降低宫颈癌细胞增殖、侵袭和有氧糖酵解(P<0.05);荧光素酶报告基因证实CYTOR可竞争性吸附miR-125b-5p,而miR-125b-5p可负调控HK2的表达。研究表明,CYTOR/miR-125b-5p/HK2分子轴促进宫颈癌细胞增殖、侵袭和有氧糖酵解,是一个潜在的宫颈癌治疗分子靶点。

To investigate the effect of lncRNA CYTOR/miR-125b-5p/HK2 axis on proliferation and invasion of cervical cancer cells,cervical cancer tissues and cells were selected to detect the expression level of CYTOR;after inhibiting CYTOR,CCK-8,Transwell,glycolysis assay was used to investigate the effects of CYTOR on proliferation,invasion and aerobic glycolysis of cervical cancer cells.The interaction between CYTOR/miR-125b-5/HK2 was verified by the dual luciferase reporter system.The results showed that CYTOR was significantly up-regulated in cervical cancer tissues and cells ( P <0.05);inhibition of CYTOR significantly decreased proliferation,invasion and aerobic glycolysis of cervical cancer cells ( P <0.05);luciferase reporter confirmed CYTOR competitively adsorbed miR-125b-5p,while miR-125b-5p negatively regulates the expression of HK2.The rescue experiment also confirmed that CYTOR increased the expression of HK2 through miR-125b-5p,which promoted the proliferation,invasion and aerobic glycolysis of cervical cancer cells ( P <0.05).Our research indicates that the CYTOR/miR-125b-5p/HK2 axis promotes proliferation,invasion and aerobic glycolysis of cervical cancer cells and is a potential molecular target for cervical cancer therapy.