Related Experiment Video
Updated: Feb 5, 2026

Orthotopic Mouse Model of Colorectal Cancer
Published on: December 4, 2007
MiR-384 inhibits the proliferation of colorectal cancer by targeting AKT3
Yong-Xia Wang1, Hui-Fang Zhu1, Zhe-Ying Zhang1
1Department of Pathology, School of Basic Medical Sciences, Xinxiang Medical University, Xinxiang, 453003 China.
Background:
Growing evidence suggests that MiRNAs play essential roles in the initiation and progression of colorectal cancer (CRC). The aberrant expression of miR-384 has been reported in some cancers. However, the role and mechanism of miR-384 in CRC proliferation remains unknown.
Methods:
The expression of miR-384 was detected in CRC and their paired normal tissues by real-time PCR. In vivo and in vitro assays were conducted to confirm the role of miR-384 in the proliferation of CRC. Bioinformatics analysis, luciferase reporter assays, western blot and in vitro assays were used to confirm that AKT3 was the target gene of miR-384. Finally, Spearman's correlation analyses was carried out to analyze the relationship between miR-384 expression and AKT3 expression in CRC.
Results:
MiR-384 was down‑regulated in CRC tissues. The in vivo and vitro functional assays verified that the ectopic upregulation of miR-384 inhibited the proliferation of CRC and the inhibition of miR-384 promoted the proliferation of CRC. Bioinformatics analysis, luciferase reporter assays, western blot and in vitro functional assays confirmed AKT3 as the target gene of miR-384. The expression of miR-384 was negatively correlated with the expressions of AKT3.
Conclusion:
Our study verified that miR-384 could significantly suppress the proliferation of CRC by directing targeting AKT3.
Related Concept Videos
Targeted Cancer Therapies
There are several types of targeted therapies against...
Feedback Inhibition
Abnormal Proliferation
Enzyme Inhibition
Inhibition of Cdk Activity
Cells Coordinate Growth and Proliferation

