Related Experiment Video
Updated: Mar 28, 2026

Analysis of Combinatorial miRNA Treatments to Regulate Cell Cycle and Angiogenesis
Published on: March 30, 2019
MiRNA-323-5p Promotes U373 Cell Apoptosis by Reducing IGF-1R
Hong-An Yang1, Xiang Wang2, Feng Ding3
1Department of Neurosurgery, Shandong Provincial Hospital Affiliated to Shandong University, Jinan, Shandong, China (mainland).
Abstract:
BACKGROUND MicroRNA regulates mammalian cell growth in terms of its proliferation and apoptosis by controlling the expression of target genes. MiRNA-323-5p plays an important role in regulating cell growth and death within various types of cells. The function of miRNA-323-5p and its possible molecular mechanism in human cerebral glioma U373 cells remains to be further confirmed. The aim of this study was to investigate the regulation function of miRNA-323-5p in human glioma U373 cell growth, proliferation, and apoptosis. MATERIAL AND METHODS We used human cerebral glioma U373 cells as the cell model; utilized liposome technology (transfected by Lipofectamine2000) in human cerebral glioma U373 cells to over-express miRNA-323-5p (microRNA used as control group); and selected MTT assay and flow cytometry to detect cell growth, proliferation, and apoptosis. We used RT-PCR and Western blotting techniques to study the expression levels of target insulin-like growth factor 1 (IGF-1) receptor protein in U373 cells transfected with miRNA-323-5p. We used liposome transfection techniques in human cerebral glioma U373 cells to over-express or processed knockdown of IGF-1R by siRNA, and then transferred with miRNA-323-5p, thereby investigating the treated human cerebral glioma U373 cells apoptosis situations. RESULTS The over-expression of miRNA-323-5p inhibited the growth and proliferation of human cerebral glioma U373 cells and promoted its apoptosis. The over-expression of miRNA-323-5p also reduced the IGF-1R level. After processing the knockdown of IGF-1R and then transfection with miRNA-323-5p, U373 cells had enhanced apoptosis. The over-expression of IGF-1R inhibited the cells apoptosis induced by miRNA-323-5p. CONCLUSIONS MiRNA-323-5p inhibited human cerebral glioma U373 cell proliferation and promoted its apoptosis by reducing IGF-1R.
Insights
MicroRNA-323-5p inhibits human glioma U373 cell growth and proliferation while promoting apoptosis. This effect is mediated by the down-regulation of the insulin-like growth factor 1 receptor (IGF-1R).
Area of Science:
- Molecular Biology
- Cell Biology
- Oncology
Background:
- MicroRNAs regulate mammalian cell growth, proliferation, and apoptosis by controlling gene expression.
- MiRNA-323-5p is implicated in cell growth and death, but its specific role in human cerebral glioma U373 cells requires clarification.
Purpose of the Study:
- To investigate the regulatory function of miRNA-323-5p in human glioma U373 cell growth, proliferation, and apoptosis.
- To elucidate the molecular mechanism underlying miRNA-323-5p's action in these cells.
Main Methods:
- Human cerebral glioma U373 cells were used as a model system.
- Liposome-mediated transfection (Lipofectamine 2000) was employed to over-express miRNA-323-5p or silence IGF-1R using siRNA.
- MTT assay, flow cytometry, RT-PCR, and Western blotting were utilized to assess cell behavior and molecular changes.
Main Results:
- Over-expression of miRNA-323-5p significantly inhibited U373 cell growth and proliferation and induced apoptosis.
- MiRNA-323-5p over-expression led to a reduction in insulin-like growth factor 1 receptor (IGF-1R) levels.
- Knockdown of IGF-1R enhanced apoptosis in miRNA-323-5p transfected cells, while IGF-1R over-expression counteracted miRNA-323-5p-induced apoptosis.
Conclusions:
- MiRNA-323-5p acts as an inhibitor of human cerebral glioma U373 cell proliferation.
- MiRNA-323-5p promotes apoptosis in U373 cells through the down-regulation of IGF-1R.
- IGF-1R is a key molecular target mediating the effects of miRNA-323-5p on glioma cell behavior.
Related Concept Videos
MicroRNAs
MicroRNAs
Abnormal Proliferation
Receptor Downregulation in MVBs
The EGFR can initiate signaling pathways that lead to cell proliferation, migration, and differentiation. Overexpression of EGFR stimulates cells to proliferate. Excessive EGFR...
Experimental RNAi
Regulation of the Unfolded Protein Response

