南方医科大学学报

南方医科大学学报 ›› 2022, Vol. 42 ›› Issue (10): 1431-1439.doi: 10.12122/j.issn.1673-4254.2022.10.01

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SOX2-OT/SOX2轴通过Gli1介导的上皮间质转化调控肺鳞癌H520细胞的迁移

董洪亮，曾莉莉，武 艳，苗 双，倪 娜，刘乃国，陈微微，杜 静   

  1. 滨州医学院附属医院医学研究中心，口腔颌面外科，山东 滨州 256600；滨州医学院口腔医学院，山东 烟台 264003
  • 出版日期:2022-10-20 发布日期:2022-10-31

SOX2-OT/SOX2 axis regulates lung cancer H520 cell migration via Gli1-mediated epithelial-mesenchymal transition

DONG Hongliang, ZENG Lili, WU Yan, MIAO Shuang, NI Na, LIU Naiguo, CHEN Weiwei, DU Jing   

  1. Medical Research Center, Department of Oral and Maxillofacial Surgery, Binzhou Medical University Hospital, Binzhou 256600, China; School of Stomatology, Binzhou Medical University, Yantai 264003, China
  • Online:2022-10-20 Published:2022-10-31

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摘要： 目的 探讨SOX2-OT在肺鳞癌细胞H520迁移能力调控中的作用并阐明其机制。方法 选用肺癌细胞株中SOX2-OT高表达的肺鳞癌细胞H520，敲低其SOX2-OT转录水平，通过细胞划痕实验和穿膜实验对细胞迁移能力进行检测，qRT-PCR和免疫印迹方法检测上皮间质转化（EMT）相关因子的表达。通过过表达Gli1进一步分析SOX2-OT的作用机制；用miR-200c抑制剂或类似物转染细胞，分析SOX2-OT对Gli的正向调控机制。结果 敲低SOX2-OT抑制了H520细胞的侵袭和迁移能力，同时伴随着细胞EMT表型的变化。SOX2-OT能够正向调控转录因子Gli1，Gli1过表达可逆转SOX2-OT敲低对细胞迁移能力的抑制作用。miR-200c抑制剂可有效逆转SOX2-OT敲低导致的SOX2下调。结论 SOX2-OT/SOX2轴通过Gli1介导的EMT过程来调控肺鳞癌细胞H520的迁移和侵袭能力。

关键词: SOX2-OT；H520细胞；Gli1；SOX2；上皮间质转化

Abstract: Objective To explore the regulatory role of SOX2-OT in migration of lung squamous cell carcinoma H520 cells and the underlying mechanisms. Methods Wound- healing and Transwell migration assays were performed to examine the changes in migration and invasion capacity of lung squamous cell line H520, which expressed higher levels of SOX2-OT than other lung cancer cell lines, following RNA interference-mediated SOX2-OT knockdown. The transcription levels of epithelial-mesenchymal transition (EMT)-related components was detected by qRT-PCR and immunoblotting. Gli1 gain-of-function analysis was performed in H520 cells with SOX2-OT knockdown and the changes in EMT phenotype of the cells were examined. miR-200c mimic and inhibitor were used to analyze the mechanism by which SOX2-OT positively regulates Gli1 and the mediating role of SOX2. Results SOX2-OT knockdown significantly lowered the invasiveness and migration capacity of H520 cells and caused changes in EMT phenotype of the cells. Overexpression of Gli1, which was positively regulated by SOX2-OT, reversed the inhibitory effect of SOX2-OT knockdown on migration of H520 cells. Transfection of the cells with miR-200c inhibitor effectively reversed SOX2-OT knockdown-induced down-regulation of SOX2. Conclusion The SOX2-OT/SOX2 axis positively regulates migration of lung squamous H520 cells via Gli1-mediated EMT.

Key words: SOX2-OT; lung squamous cell carcinoma; Gli1; SOX2; epithelial-mesenchymal transition