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Updated: Dec 8, 2025

In Vivo Inhibition of MicroRNA to Decrease Tumor Growth in Mice
Published on: August 23, 2019
MicroRNA-3690 promotes cell proliferation and cell cycle progression by altering DKK3 expression in human thyroid
Fei Shen1,2, Xiao-Xiong Gan1,2, Xing-Yan Deng1,2
1Department of Thyroid Surgery, Guangzhou First People's Hospital, Guangzhou Medical University, Guangzhou, Guangdong 510180, P.R. China.
Abstract:
An increasing amount of evidence has demonstrated the importance of microRNAs (miRNAs/miRs) in the tumorigenesis of malignant types of cancer, and data retrieved from The Cancer Genome Atlas database revealed that miR-3690 was upregulated in thyroid cancer (TC). The present study focused on the biological function and mechanism of miR-3690 in TC, demonstrating that miR-3690 expression was significantly elevated in TC cells and clinical tissues. Functional studies indicated that miR-3690 acted as an oncogene in TC by promoting cell proliferation, colony formation and cell cycle progression in association with the increased expression of cyclin E and c-myc. Mechanistically, prediction software indicated that Dickkopf-related protein 3 (DKK3) was a target of miR-3690, which was confirmed by the results of luciferase reporter assays and western blotting. DKK3 silencing abrogated the functions of miR-3690-in on TC cell proliferation. Collectively, the findings of the present study demonstrated that miR-3690 promoted TC cell proliferation and indicated miR-3690 as a potential biomarker and therapeutic target for TC.
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