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MiR-494 Inhibits Epithelial Ovarian Cancer Growth by Targeting c-Myc
BACKGROUND: Epithelial ovarian cancer (EOC) is the most lethal malignant gynecological cancer. MicroRNAs (miRNAs) play important roles in the pathogenesis of ovarian cancer. The role of miR-494 in EOC has not been fully investigated. MATERIAL/METHODS: MiR-494 levels in ovarian cancer tissues and cel...
Autores principales: | , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
International Scientific Literature, Inc.
2016
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4768945/ https://www.ncbi.nlm.nih.gov/pubmed/26908019 http://dx.doi.org/10.12659/MSM.897288 |
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author | Yuan, Jialing Wang, Kana Xi, Mingrong |
author_facet | Yuan, Jialing Wang, Kana Xi, Mingrong |
author_sort | Yuan, Jialing |
collection | PubMed |
description | BACKGROUND: Epithelial ovarian cancer (EOC) is the most lethal malignant gynecological cancer. MicroRNAs (miRNAs) play important roles in the pathogenesis of ovarian cancer. The role of miR-494 in EOC has not been fully investigated. MATERIAL/METHODS: MiR-494 levels in ovarian cancer tissues and cells were tested by qRT-PCR. Cells were transfected with miR-494 mimics or miR-494 ASO by Lipofectamine. Bioinformatics algorithms from TargetScanHuman were used to predict the target genes of miR-494. The c-Myc protein level was assayed by Western blot. The interaction between miR-494 and c-Myc was confirmed by dual luciferase assays. RESULTS: MiR-494 showed low levels in EOC tissues and cells. Overexpression of miR-494 inhibited cell growth and migration of EOC cells and vice versa. c-Myc is the targeted gene of miR-494. CONCLUSIONS: MiR-494 has an anti-tumor role in EOC via c-Myc. |
format | Online Article Text |
id | pubmed-4768945 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2016 |
publisher | International Scientific Literature, Inc. |
record_format | MEDLINE/PubMed |
spelling | pubmed-47689452016-03-10 MiR-494 Inhibits Epithelial Ovarian Cancer Growth by Targeting c-Myc Yuan, Jialing Wang, Kana Xi, Mingrong Med Sci Monit Lab/In Vitro Research BACKGROUND: Epithelial ovarian cancer (EOC) is the most lethal malignant gynecological cancer. MicroRNAs (miRNAs) play important roles in the pathogenesis of ovarian cancer. The role of miR-494 in EOC has not been fully investigated. MATERIAL/METHODS: MiR-494 levels in ovarian cancer tissues and cells were tested by qRT-PCR. Cells were transfected with miR-494 mimics or miR-494 ASO by Lipofectamine. Bioinformatics algorithms from TargetScanHuman were used to predict the target genes of miR-494. The c-Myc protein level was assayed by Western blot. The interaction between miR-494 and c-Myc was confirmed by dual luciferase assays. RESULTS: MiR-494 showed low levels in EOC tissues and cells. Overexpression of miR-494 inhibited cell growth and migration of EOC cells and vice versa. c-Myc is the targeted gene of miR-494. CONCLUSIONS: MiR-494 has an anti-tumor role in EOC via c-Myc. International Scientific Literature, Inc. 2016-02-24 /pmc/articles/PMC4768945/ /pubmed/26908019 http://dx.doi.org/10.12659/MSM.897288 Text en © Med Sci Monit, 2016 This work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivs 3.0 Unported License |
spellingShingle | Lab/In Vitro Research Yuan, Jialing Wang, Kana Xi, Mingrong MiR-494 Inhibits Epithelial Ovarian Cancer Growth by Targeting c-Myc |
title | MiR-494 Inhibits Epithelial Ovarian Cancer Growth by Targeting c-Myc |
title_full | MiR-494 Inhibits Epithelial Ovarian Cancer Growth by Targeting c-Myc |
title_fullStr | MiR-494 Inhibits Epithelial Ovarian Cancer Growth by Targeting c-Myc |
title_full_unstemmed | MiR-494 Inhibits Epithelial Ovarian Cancer Growth by Targeting c-Myc |
title_short | MiR-494 Inhibits Epithelial Ovarian Cancer Growth by Targeting c-Myc |
title_sort | mir-494 inhibits epithelial ovarian cancer growth by targeting c-myc |
topic | Lab/In Vitro Research |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4768945/ https://www.ncbi.nlm.nih.gov/pubmed/26908019 http://dx.doi.org/10.12659/MSM.897288 |
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