Related Experiment Video
Updated: Nov 23, 2025

An In Vitro Protocol for Evaluating MicroRNA Levels, Functions, and Associated Target Genes in Tumor Cells
Published on: May 21, 2019
miR-21-5p promotes cell proliferation by targeting BCL11B in Thp-1 cells
Liang Zhang1, Li Yu1, Yiran Liu1
1Shandong Provincial Key Laboratory of Animal Resistance Biology, Institute of Biomedical Sciences, College of Life Sciences, Shandong Normal University, Jinan, Shandong 250014, P.R. China.
Abstract:
Acute myeloid leukemia (AML) is a highly heterogeneous disease that remains untreatable. MicroRNAs (miRNAs or miRs) play important roles in the pathogenesis of leukemia. miR-21 is highly expressed in multiple types of human cancer and displays oncogenic activities; however, the clinical significance of miR-21 in AML remains unclear. In the present study, it was demonstrated that miR-21 levels were high in patients with AML and in AML cell lines. Further experiments demonstrated that overexpression of miR-21 in Thp-1 human monocytes derived from acute mononuclear leukemia peripheral blood promoted cell proliferation, while downregulation of miR-21-5p, a mature sequence derived from the 5' end of the miR-21 stem-loop precursor (another mature sequence, miR-21-3p, is derived form 3' end of miR-21), inhibited cell proliferation. Specifically, it was observed that overexpression of miR-21 could promote the transition of Thp-1 cells into the S and G2/M phases of the cell cycle, as shown by flow cytometry. Furthermore, inhibition of miR-21-5p arrested cells in the S and G2/M phases. Finally, BCL11B was determined to be a functional target of miR-21-5p by luciferase assays. Our study revealed functional and mechanistic associations between miR-21 and BCL11B in Thp-1 cells, which could serve to guide clinical treatment of AML.
Related Concept Videos
Abnormal Proliferation
mTOR Signaling and Cancer Progression
The mTOR pathway or the...
Targeted Cancer Therapies
There are several types of targeted therapies against...
Mitogens and the Cell Cycle
TGF - β Signaling Pathway
Negative Regulator Molecules

