首页|长链非编码RNA RMST通过靶向微小RNA-24-3p抑制口腔鳞癌细胞增殖、迁移和侵袭

长链非编码RNA RMST通过靶向微小RNA-24-3p抑制口腔鳞癌细胞增殖、迁移和侵袭

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目的:探讨长链非编码RNA横纹肌肉瘤2相关转录本(lncRNA RMST)和微小RNA-24-3p(miR-24-3p)在口腔鳞状细胞癌细胞(OSCCs)增殖、迁移和侵袭中的作用.方法:生物信息学UALCAN数据库分析头颈部鳞状细胞癌(HNSC)组织中RMST的表达.实时荧光定量PCR(qRT-PCR)检测RMST和miR-24-3p在5个人OSCC细胞系中的表达.将体外培养的CAL27 细胞分为:control 组、pcDNA3.1 组(空载体)、pcDNA3.1-RMST+mimics-NC 组(过表达 RMST+miR-24-3p 阴性对照)和pcDNA3.1-RMST+miR-24-3p mimics 组(过表达 RMST+miR-24-3p).双荧光素酶基因报告实验分析 RMST 与 miR-24-3p 之间的相互作用关系.MTT比色法、划痕实验和Transwell实验用于检测细胞增殖、迁移和侵袭.Western blot和qRT-PCR法检测E-cadherin,N-cadherin和c-myc表达.结果:RMST在OSCC组织和细胞表达水平下降(P<0.01),miR-24-3p在OSCC细胞表达水平上升(P<0.01),是RMST的潜在靶基因.pcDNA3.1-RMST组miR-24-3p水平低于pcDNA3.1组(P<0.01).pcD-NA3.1-RMST+mimics-NC 组细胞的增殖、迁移和侵袭低于 pcDNA3.1 组(P<0.01),而 pcDNA3.1-RMST+miR-24-3p mimics 组细胞的增殖、迁移和侵袭高于 pcDNA3.1-RMST+mimics-NC 组(P<0.01).与 pcDNA3.1 组相比,pcDNA3.1-RMST+mimics-NC组 E-cadherin 表达更高、N-cadherin 和 c-myc 表达更低(P<0.01);与 pcDNA3.1-RMST+mimics-NC 组相比,pcDNA3.1-RMST+miR-24-3p mimics 组 E-cadherin 表达更低、N-cadherin 和 c-myc 表达更高(P<0.01).结论:OSCC 中低表达的RMST通过靶向miR-24-3p抑制细胞的增殖、迁移和侵袭进程.
Long non-coding RNA RMST inhibits cell proliferation,migration and invasion by targeting microRNA-24-3p in OSCCs
Objective:To explore the role of long non-coding RNA rhabdomyosarcoma 2 associated transcript(lncRNA RMST)and microRNA-24-3p(miR-24-3p)in proliferation,migration and invasion of oral squamous cell carcinoma cells(OSCCs).Methods:The RMST expression in head and neck squamous cell carcinoma(HNSC)was analyzed by UALCAN data base.qRT-PCR was used to detect the expression of RMST and miR-24-3p in 5 human OSCC cell lines.CAL27 cells were in vitro cultured and allocated into con-trol group,pcDNA3.1 group(vector),pcDNA3.1-RMST+mimics-NC group(overexpression of RMST+negative control of miR-24-3p)and pcDNA3.1-RMST+miR-24-3p mimics group(overexpression of RMST+miR-24-3p).Dual luciferase reporter assay was per-formed to analyze the interaction between RMST and miR-24-3p.MTT assay,wound-healing and transwell assay were applied to de-tect the proliferation,migration and invasion of the cells.Western blot and qRT-PCR were conducted to measure the expression of E-cadherin,N-cadherin and c-myc in the cells.Results:RMST level were down-regulated in HNSC tissues and OSCC cell lines(P<0.01).While miR-24-3p level was elevated in OSCC cell lines(P<0.01).miR-24-3p was identified and confirmed as a potential binding partner to RMST.miR-24-3p level was lower in pcDNA3.1-RMST group than in pcDNA3.1 group(P<0.01).The prolifera-tion,migration and invasion abilities of CAL27 cell in pcDNA3.1-RMST+mimics-NC group were lower than in pcDNA3.1 group(P<0.01).While those of CAL27 cells in pcDNA3.1-RMST+miR-24-3p mimics group were higher than in pcDNA3.1-RMST+mimics-NC group(P<0.01).Compared with pcDNA3.1 group,pcDNA3.1-RMST+miR-24-3p mimics showed higher expression of E-cad-herin,lower expression of N-cadherin and c-myc(P<0.01).Compared with pcDNA3.1-RMST+miR-24-3p mimics group,pcD-NA3.1-RMST+miR-24-3p mimics group showed lower expression of E-cadherin,higher expression of N-cadherin and c-myc(P<0.01).Conclusion:Down-expressed RMST may suppress the proliferation,migration and invasion progression of OSCC cells through targeting miR-24-3p.

RMSTOral squamous cell carcinomamiR-24-3pMigrationInvasion

李逸舒、屠淑贞

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215200,苏州市第九人民医院口腔科

RMST OSCC miR-24-3p 迁移 侵袭

2024

实用口腔医学杂志
第四军医大学口腔医学院

实用口腔医学杂志

CSTPCD北大核心
影响因子:0.942
ISSN:1001-3733
年,卷(期):2024.40(1)
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