中国临床解剖学杂志 ›› 2023, Vol. 41 ›› Issue (2): 194-199.doi: 10.13418/j.issn.1001-165x.2023.2.13

• 实验研究 • 上一篇    下一篇

微小RNA-3651过表达通过介导核因子κB信号通路抑制人舌癌细胞CAL27的生长与侵袭

吕艳利1,     巴凯2,    方政2   

  1. 1.洛阳职业技术学院教研室,  河南   洛阳    471000;    2.郑州大学第一附属医院口腔颌面外科,  郑州   450100
  • 收稿日期:2021-12-06 出版日期:2023-03-25 发布日期:2023-04-14
  • 作者简介:吕艳利(1980-),女,河南洛阳人,本科,高校讲师,主要从事口腔颌面外科疾病研究,E-mail:Lvyanli123123@163.com
  • 基金资助:
    国家自然科学基金(81500826)

microRNA-3651 overexpression inhibiting the growth and invasion of human tongue cancer CAL27 cells by mediating nuclear factor κB signaling pathway

Lv Yanli1 , Ba Kai2, Fang Zheng2   

  1. 1. Teaching and Research Office, Luoyang Vocational and Technical College, Luoyang 471000, China; 2. Department of Oral and Maxillofacial Surgery, The First Affiliated Hospital of Zhengzhou University, Zhengzhou 450100, China
  • Received:2021-12-06 Online:2023-03-25 Published:2023-04-14

摘要: 目的    探讨微小RNA(miR)-3651过表达通过介导核因子(NF)-κB信号通路抑制人舌癌细胞CAL27生长与侵袭的机制。  方法    将对数生长期CAL27细胞分为miR-3651 mimic组、mimic-NC组和对照组。采用qRT-PCR检测转染后细胞miR-3651水平,CCK-8检测细胞活力,Transwell检测细胞侵袭能力,划痕实验检测细胞迁移能力,光学显微镜下观察细胞上皮间质转化(epithelial-mesenchymal transition,EMT)的形成,Western blot检测E钙粘蛋白、N钙粘蛋白、波形蛋白、NF-κB p65和p-NF-κB p65蛋白表达。  结果    mimic-NC组与对照组细胞miR-3651水平、细胞活力、侵袭细胞数、细胞迁移率和细胞形态均无明显差异(P>0.05),E钙粘蛋白、N钙粘蛋白、波形蛋白和p-NF-κB p65/NF-κB p65蛋白表达均无明显差异(P>0.05);与mimic-NC组相比,miR-3651 mimic组细胞miR-3651水平升高(P<0.05),培养的细胞第2、3、4 天的活力降低(P<0.05),侵袭细胞数和细胞迁移率降低(P<0.05),细胞E钙粘蛋白表达升高(P<0.05),N钙粘蛋白、波形蛋白和p-NF-κB p65/NF-κB p65蛋白表达下降(P<0.05),显微镜下观察到EMT形成减少。  结论    过表达miR-3651可以抑制CAL27细胞的生长和侵袭,其作用机制可能与抑制NF-κB信号通路磷酸化有关。

关键词: 微小RNA-3651; ,  , 核因子κB; ,  , 舌癌; ,  , 侵袭

Abstract: Objective    To explore the mechanism of microRNA (miR)-3651 overexpression on inhibiting the growth and invasion of human tongue cancer CAL27 cells by mediating nuclear factor (NF)-κB signaling pathway.     Methods    CAL27 cells in logarithmic growth phase were divided into a miR-3651 mimic group, a mimic-NC group and a control group. The level of miR-3651 in each group after transfection was detected by fluorescent quantitative real-time polymerase chain reaction (qRT-PCR). The cell vitality in each group was detected by cell counting kit-8 (CCK-8). The invasion ability of cells in each group was detected by Transwell. The migration ability of cells in each group was detected by scratch assay. The formation of epithelial-mesenchymal transition (EMT) in each group was observed under light microscope. The expression of E-cadherin, N-cadherin, Vimentin, NF-κB p65 and p-NF-κB p65 was detected by Western Blot.    Results    There was no  statistically significant difference in miR-3651 level, activity of cells vitality, number of invasion cells, cells migration rate and cells morphology between mimic-NC group and control group (P>0.05), and there was no significant difference in the expression of E-cadherin, N-cadherin, Vimentin and p-NF-κB p65/NF-κB p65 proteins (P>0.05). Compared with the mimic-NC group, in the miR-3651 mimic group, miR-3651 level was significantly increased (P<0.05), cells vitality were significantly decreased at 2d, 3d, 4d after cell culture (P<0.05), number of invasion cells and cells migration rate were significantly decreased (P<0.05), expression of E-cadherin protein was significantly increased (P<0.05), expression of N-cadherin, Vimentin and p-NF-κB p65/NF-κB p65 proteins were significantly decreased (P<0.05), and EMT formation under microscope was decreased.   Conclusions   miR-3651 overexpression can inhibit the growth and invasion of CAL27 cells, and its action mechanism may be related to the inhibiting the phosphorylation of NF-κB signaling pathway.

Key words:  microRNA-3651; ,  , Nuclear factor κB; ,  ,  Tongue cancer; ,  ,  Invasion

中图分类号: