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Hong-an Yang, Xiang Wang, Feng Ding, Qi Pang
(Department of Neurosurgery, Shandong Provincial Hospital Affiliated to Shandong University, Jinan, Shandong, China (mainland))
Med Sci Monit 2015; 21:3880-3886
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.