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Updated: Oct 28, 2025

In Vivo Inhibition of MicroRNA to Decrease Tumor Growth in Mice
Published on: August 23, 2019
Long-chain non-coding RNA HOTTIP enhances oral cancer cell proliferation and migration capacity by down-regulating
1Department of Stomatology, Hospital of Shandong University, Jinan, China.
Purpose:
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.
Methods:
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.
Results:
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.
Conclusions:
HOTTIP promotes the tumor proliferation activity and migration of oral cancer cells through modulating miR-206.
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