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lncRNA SNHG14通过miR-217-5p/FHIT分子轴抑制膀胱癌细胞的增殖和侵袭能力 被引量:4

Long-chain non-coding RNA SNHG14 inhibits proliferation and invasion of bladder cancer cells via miR-217-5p/FHIT molecular axis
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摘要 目的探讨长链非编码RNA(long-chain non-coding RNA,lncRNA)SNHG14在膀胱癌组织的表达及其抑制膀胱癌细胞增殖和侵袭能力的分子机制。方法实时荧光定量聚合酶链反应(qRT-PCR)检测SNHG14在75例膀胱癌组织及癌旁组织、膀胱癌细胞株及正常膀胱上皮细胞中的表达量。以表达量最低的BIU-87细胞为对象,分别转染阴性对照质粒或SNHG14高表达质粒,定义为对照组和实验组。MTT法、Matrigel侵袭实验检测高表达SNHG14对BIU-87细胞增殖、侵袭能力的影响。生物信息学技术预测SNHG14作用的分子机制。qRT-PCR和Western Blot检测高表达SNHG14对下游基因表达的影响。结果 SNHG14在膀胱癌组织中的表达显著低于癌旁组织(P <0.01)。SNHG14在膀胱癌细胞株中的表达显著低于正常膀胱上皮细胞(P <0.01)。高表达SNHG14可抑制BIU-87细胞的增殖能力(P <0.05)和侵袭能力(P <0.05)。生物信息学技术显示,SNHG14可互补结合miR-217-5p,miR-217-5p可互补结合脆性组氨酸三联体(fragile histidine teiad,FHIT)。高表达SNHG14明显降低BIU-87细胞中miR-217-5p的表达(P <0.01),明显促进FHIT mRNA和蛋白的表达(P <0.01)。结论 SNHG14在膀胱癌组织和细胞株中表达显著降低,高表达SNHG14可显著抑制膀胱癌BIU-87细胞的增殖和侵袭能力,其分子机制可能是抑制miR-217-5p的表达、促进FHIT基因的表达。 Objective To investigate the expression of long-chain non-coding RNA(lncRNA)SNHG14 inbladder cancer tissues and its molecular mechanism of inhibiting the proliferation and invasion of bladder cancercells.MethodsReal-time quantitative polymerase chain reaction(q RT-PCR)was used to detect the expression ofSNHG14 in 75 bladder cancer tissues and adjacent tissues,bladder cancer cells and normal bladder epithelial cells.The BIU-87 cells with the lowest expression rate were transfected into the negative control plasmid or the SNHG14 high expression plasmid,which were defined as the control group and the experimental group. MTT assay and Matrigelinvasion assay were used to detect the effect of high expression of SNHG14 on proliferation and invasion of BIU-87 cells. Bioinformatics technology predicts the molecular mechanism of the role of SNHG14. q RT-PCR and WesternBlot were used to detect the effect of high expression of SNHG14 on downstream gene expression.ResultTheexpression of SNHG14 in bladder cancer tissues was significantly lower than that in adjacent tissues(P < 0.01). Theexpression of SNHG14 in bladder cancer cell lines was significantly lower than that in normal bladder epithelial cells(P < 0.01). High expression of SNHG14 inhibited the proliferation of BIU-87 cells(P < 0.05)and invasive ability(P < 0.05). Bioinformatics technology showed that SNHG14 could complement the miR-217-5p,and miR-217-5pcould complement the fragile histidine triad(FHIT). High expression of SNHG14 significantly decreased the ex-pression of miR-217-5p in BIU-87 cells(P < 0.01),and significantly promoted the expression of FHIT m RNA andprotein(P < 0.01).ConclusionsThe expression of SNHG14 is significantly decreased in bladder cancer tissues andcell lines. High expression of SNHG14 significantly inhibits the proliferation and invasion of bladder cancer cell lineBIU-87. The molecular mechanism may inhibit the expression of miR-217-5p and promote the FHIT gene expression.
作者 鲁帅奇 杨凌博 秦帅锋 张寒 孙建涛 LU Shuaiqi;YANG Lingbo;QIN Shuaifeng;ZHANG Han;SUN Jiantao(Department of Urology,Luoyang Central Hospital,Zhengzhou University,Luoyang 471009,China)
出处 《实用医学杂志》 CAS 北大核心 2020年第14期1903-1907,共5页 The Journal of Practical Medicine
基金 河南省医学科技攻关计划(编号:2018020895)。
关键词 膀胱癌 长链非编码RNA miR-217-5p 脆性组氨酸三联体 bladder cancer long-chain non-coding RNA miR-217-5p fragile histidine teiad
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