Department of Stomatology, Hospital of Shandong University, Jinan, China.
J BUON. 2021 May-Jun;26(3):762-768.
The purpose of this study was to explore the specific role and potential mechanism of long non-coding RNA HOTTIP in the progression of oral cancer.
HOTTIP in oral cancer tissues and adjacent normal tissues was measured by quantitative real-time polymerase chain reaction (qRT- PCR) technology. After knockdown of HOTTIP expression in oral cancer cell lines, Cell Counting Kit (CCK-8), scratch healing experiment, and Transwell assay were carried out to explore cell proliferation and migration capacity. Furthermore, in order to discover the underlying mechanism, a dual luciferase experiment was designed to verify the binding of HOTTIP to the downstream miR-206 based on the prediction results of the bioinformatics prediction website. Finally, we designed a cell function recovery experiment using co-transfection technology to further confirm the regulation of HOTTIP on miR-206.
HOTTIP was abnormally increased in oral cancer. At the same time, the survival analysis showed that the higher expression of HOTTIP was significantly correlated with a shorter overall survival. The results of cell functional experiments found that HOTTIP played a role in promoting tumor proliferation and migration in oral cancer cells. Besides, when HOTTIP was knocked down in oral cancer cell lines, miR-206-206 was remarkably up-regulated. Dual-luciferase reporter gene experiment confirmed the binding relationship between miR-206 and HOTTIP. In addition, miR-206 was found to be differently expressed in oral cancer tissues from that in normal control tissues. Cellular function experiments verified that HOTTIP could promote tumor proliferation activity and migration by altering miR-206 in oral cancer.
HOTTIP promotes the tumor proliferation activity and migration of oral cancer cells through modulating miR-206.
本研究旨在探讨长链非编码 RNA HOTTIP 在口腔癌进展中的具体作用和潜在机制。
采用实时定量聚合酶链反应（qRT-PCR）技术检测口腔癌组织及相邻正常组织中 HOTTIP 的表达。敲低口腔癌细胞系中 HOTTIP 的表达后，通过细胞计数试剂盒（CCK-8）、划痕愈合实验和 Transwell 实验来探讨细胞增殖和迁移能力。此外，为了发现潜在的机制，设计了双荧光素酶实验，基于生物信息学预测网站的预测结果来验证 HOTTIP 与下游 miR-206 的结合。最后，通过共转染技术设计细胞功能恢复实验，进一步证实 HOTTIP 对 miR-206 的调控作用。
HOTTIP 在口腔癌中异常升高。同时，生存分析表明 HOTTIP 表达越高，总生存期越短。细胞功能实验结果发现 HOTTIP 在口腔癌细胞中发挥促进肿瘤增殖和迁移的作用。此外，当在口腔癌细胞系中敲低 HOTTIP 时，miR-206 显著上调。双荧光素酶报告基因实验证实了 miR-206 与 HOTTIP 之间的结合关系。此外，还发现 miR-206 在口腔癌组织中的表达与正常对照组织不同。细胞功能实验验证了 HOTTIP 通过改变 miR-206 促进口腔癌细胞的肿瘤增殖活性和迁移。
HOTTIP 通过调节 miR-206 促进口腔癌细胞的肿瘤增殖活性和迁移。
