ArticleOncology letters2019
Expression of miR-664 and miR-184 on proliferation, apoptosis and migration of osteosarcoma cells.
Article in Oncology letters, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed.
- miR-184 in hepatocellular carcinoma: a promising therapeutic target.Journal of physiology and biochemistry · 2025Review
- MicroRNA expression alteration in chronic thromboembolic pulmonary hypertension: A systematic review.Pulmonary circulation · 2024Article
- microRNA-184 in the landscape of human malignancies: a review to roles and clinical significance.Cell death discovery · 2023Review
- MicroRNA as a Prognostic and Diagnostic Marker in T-Cell Acute Lymphoblastic Leukemia.International journal of molecular sciences · 2021Review
- Analysis of a Preliminary microRNA Expression Signature in a Human Telangiectatic Osteogenic Sarcoma Cancer Cell Line.International journal of molecular sciences · 2021Article
- RNA Sequencing of Osteosarcoma Gene Expression Profile Revealed that miR-214-3p Facilitates Osteosarcoma Cell Proliferation via Targeting Ubiquinol-Cytochrome c Reductase Core Protein 1 (UQCRC1).Medical science monitor : international medical journal of experimental and clinical research · 2019Article
Corrections and comments
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Authors and funding
8 authors.
Funding
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Abstract
The expression of micro-ribonucleic acid miR-664 and miR-184 on the biological characteristics of osteosarcoma (OS) SOSP-9607 cells was investigated. Eighteen surgical specimens of OS and 18 normal tissue specimens were collected. The expression of miR-664 and miR-184 was detected via fluorescence reverse transcription-quantitative polymerase chain reaction (RT-qPCR). The OS cell line SOSP-9607 was selected as the object of study, and miR-664 blank group, miR-664 mimic group, miR-664 inhibitor group, miR-184 blank group, miR-184 mimic group and miR-184 inhibitor group were established through transfection. Changes in apoptosis were detected via flow cytometry, the cell proliferation capacity was detected via Cell Counting Kit-8 assay, and the cell migration was observed via wound healing assay. In cancer tissues of OS patients, the relative expression of miR-664 and miR-184 was significantly higher than that in para-carcinoma tissues (P<0.05). The cell growth in miR-664 inhibitor group was obviously decreased compared with those in miR-664 blank and mimic groups (P<0.05). There were differences in the cell migration capacity among groups (P<0.01), and the cell scratch areas in miR-664 and miR-184 mimic groups were significantly decreased compared with those in miR-664 and miR-184 blank groups (P<0.05), while they were significantly increased in miR-664 and miR-184 inhibitor groups compared with those in miR-664 and miR-184 blank and mimic groups (P<0.05, P<0.01). There were differences in the apoptosis rate among groups (P<0.01) and apoptosis in miR-664 and miR-184 inhibitor groups was remarkably increased compared with those in miR-664 and miR-184 blank and mimic groups (P<0.05). Downregulating the expression of miR-664 and miR-184 may promote apoptosis, inhibit the proliferation and reduce the migration capacity of SOSP-9607 cells. Therefore, miR-664 and miR-184 may provide a theoretical basis for the target selection in clinical targeted therapy and drug development for OS.
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