ArticleMedical science monitor : international medical journal of experimental and clinical research2015
MiRNA-323-5p Promotes U373 Cell Apoptosis by Reducing IGF-1R.
Article in Medical science monitor : international medical journal of experimental and clinical research, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 14 citations in OpenAlex.
- Beyond Repetition: The Role of Gray Zone Alleles in the Upregulation ofInternational journal of molecular sciences · 2025Article
- Methods of miRNA delivery and possibilities of their application in neuro-oncology.Non-coding RNA research · 2023Review
- Spectrum of microRNAs and their target genes in cancer: intervention in diagnosis and therapy.Molecular biology reports · 2022Review
- MicroRNA-3200-3p targeting CAMK2A modulates the proliferation and metastasis of gliomaBioengineered · 2022Article
- miRNA-21 plays an important role in necrotizing enterocolitis.Archives of medical science : AMS · 2022Article
- Pentose Phosphate Pathway Regulates Tolerogenic Apoptotic Cell Clearance and Immune Tolerance.Frontiers in immunology · 2021Article
- MicroRNA-421 improves ischemia/reperfusion injury via regulation toll-like receptor 4 pathway.The Journal of international medical research · 2020Article
- Prognostic and Therapeutic Roles of the Insulin Growth Factor System in Glioblastoma.Frontiers in oncology · 2020Review
- Functional high-throughput screening reveals miR-323a-5p and miR-342-5p as new tumor-suppressive microRNA for neuroblastoma.Cellular and molecular life sciences : CMLS · 2019Article
- Combined Blockade of T Cell Immunoglobulin and Mucin Domain 3 and Carcinoembryonic Antigen-Related Cell Adhesion Molecule 1 Results in Durable Therapeutic Efficacy in Mice with Intracranial Gliomas.Medical science monitor : international medical journal of experimental and clinical research · 2017Article
- Identification of IGF-1-enhanced cytokine expressions targeted by miR-181d in glioblastomas via an integrative miRNA/mRNA regulatory network analysis.Scientific reports · 2017Article
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
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.
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