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Updated: Oct 29, 2025

In Vivo Inhibition of MicroRNA to Decrease Tumor Growth in Mice
Published on: August 23, 2019
MiR-186-3p attenuates tumorigenesis of cervical cancer by targeting IGF1
Xiurong Lu1, Xiao Song2, Xiaohui Hao2
1Department of Radiotherapy, The First Affiliated Hospital of Hebei North University, No. 36, Changqing Road, Zhangjiakou, 075000, Hebei, China. xiurong_lu2@163.com.
Background:
Mounting evidence in the cancer literature suggests that microRNAs (miRNAs) influence the progression of human cancer cells by targeting protein-coding genes. How insulin-like growth factor 1(IGF1) and miR-186-3p contribute to the development of cervical cancer (CC) remains unclear. This study examined the regulatory roles of miR-186-3p and IGF1 in CC development.
Methods:
Gene expression levels were determined by qRT-PCR. Proliferation, migration, and apoptosis of CC and normal cells were determined by MTT, Transwell, and caspase-3 activity assays, respectively. Dual-luciferase reporter activity and RNA pull-down assays were performed to identify the target gene of miR-186-3p.
Results:
IGF1 was the target of miR-186-3p. The expression of miR-186-3p inhibited cell proliferation and migration abilities of CC cell lines, but induced the apoptosis rate of CC cells. IGF1 could restore the inhibitory effects of miR-186-3p on the proliferation, migration, and apoptosis abilities of CC cells. Experimental results revealed that miR-186-3p could inhibit IGF1 expression, thereby reducing the viability of CC cells.
Conclusions:
The data suggest that targeting of IGF1 by miR-186-3p could be crucial in regulating the progression of CC.
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