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MicroRNA-150 suppresses p27(Kip1) expression and promotes cell proliferation in HeLa human cervical cancer cells
MicroRNAs (miRNAs) exert critical roles in the majority of biological and pathological processes. Recent studies have associated miR-150 with a number of different cancer types. However, little is known about miR-150 targets in cervical cancer. In the present study, the HeLa human cervical cancer ce...
Autores principales: | , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
D.A. Spandidos
2020
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7491037/ https://www.ncbi.nlm.nih.gov/pubmed/32963616 http://dx.doi.org/10.3892/ol.2020.12073 |
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author | Oboshi, Wataru Hayashi, Keisuke Takeuchi, Hiroaki Ikeda, Katsuhide Yamaguchi, Yoshitaka Kimura, Asako Nakamura, Takehiro Yukimasa, Nobuyasu |
author_facet | Oboshi, Wataru Hayashi, Keisuke Takeuchi, Hiroaki Ikeda, Katsuhide Yamaguchi, Yoshitaka Kimura, Asako Nakamura, Takehiro Yukimasa, Nobuyasu |
author_sort | Oboshi, Wataru |
collection | PubMed |
description | MicroRNAs (miRNAs) exert critical roles in the majority of biological and pathological processes. Recent studies have associated miR-150 with a number of different cancer types. However, little is known about miR-150 targets in cervical cancer. In the present study, the HeLa human cervical cancer cell line was transfected with hsa-miR-150-5p mimics, hsa-miR-150-5p inhibitors or miRNA controls. miR-150 was predicted to bind the 3′untranslated region (3′UTR) of the CDKN1B gene, which encodes the cyclin-dependent kinase inhibitor 1B (p27(Kip1)). The direct binding between miR-150 and the 3′UTR of CDKN1B was confirmed using dual-luciferase reporter assays. The effects of miR-150 on CDKN1B mRNA expression, p27(Kip1) protein expression, cell cycle and cell proliferation were determined using reverse-transcription quantitative PCR, western blot analysis, flow cytometry and WST-8 assays, respectively. miR-150 was demonstrated to directly target the 3′UTR of CDKN1B in transfected HeLa cells. The expression of CDKN1B mRNA and p27(Kip1) protein was reduced by miR-150 mimics, and increased by miR-150 inhibitors. Moreover, the overexpression of miR-150 promoted cell cycle progression from the G0/G1 to the S phase and led to a significant increase in HeLa cell proliferation. The results of the present study indicated that miR-150 promotes HeLa cell cycle progression and proliferation via the suppression of p27(Kip1) expression. |
format | Online Article Text |
id | pubmed-7491037 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2020 |
publisher | D.A. Spandidos |
record_format | MEDLINE/PubMed |
spelling | pubmed-74910372020-09-21 MicroRNA-150 suppresses p27(Kip1) expression and promotes cell proliferation in HeLa human cervical cancer cells Oboshi, Wataru Hayashi, Keisuke Takeuchi, Hiroaki Ikeda, Katsuhide Yamaguchi, Yoshitaka Kimura, Asako Nakamura, Takehiro Yukimasa, Nobuyasu Oncol Lett Articles MicroRNAs (miRNAs) exert critical roles in the majority of biological and pathological processes. Recent studies have associated miR-150 with a number of different cancer types. However, little is known about miR-150 targets in cervical cancer. In the present study, the HeLa human cervical cancer cell line was transfected with hsa-miR-150-5p mimics, hsa-miR-150-5p inhibitors or miRNA controls. miR-150 was predicted to bind the 3′untranslated region (3′UTR) of the CDKN1B gene, which encodes the cyclin-dependent kinase inhibitor 1B (p27(Kip1)). The direct binding between miR-150 and the 3′UTR of CDKN1B was confirmed using dual-luciferase reporter assays. The effects of miR-150 on CDKN1B mRNA expression, p27(Kip1) protein expression, cell cycle and cell proliferation were determined using reverse-transcription quantitative PCR, western blot analysis, flow cytometry and WST-8 assays, respectively. miR-150 was demonstrated to directly target the 3′UTR of CDKN1B in transfected HeLa cells. The expression of CDKN1B mRNA and p27(Kip1) protein was reduced by miR-150 mimics, and increased by miR-150 inhibitors. Moreover, the overexpression of miR-150 promoted cell cycle progression from the G0/G1 to the S phase and led to a significant increase in HeLa cell proliferation. The results of the present study indicated that miR-150 promotes HeLa cell cycle progression and proliferation via the suppression of p27(Kip1) expression. D.A. Spandidos 2020-11 2020-09-08 /pmc/articles/PMC7491037/ /pubmed/32963616 http://dx.doi.org/10.3892/ol.2020.12073 Text en Copyright: © Oboshi et al. This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License (https://creativecommons.org/licenses/by-nc-nd/4.0/) , which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made. |
spellingShingle | Articles Oboshi, Wataru Hayashi, Keisuke Takeuchi, Hiroaki Ikeda, Katsuhide Yamaguchi, Yoshitaka Kimura, Asako Nakamura, Takehiro Yukimasa, Nobuyasu MicroRNA-150 suppresses p27(Kip1) expression and promotes cell proliferation in HeLa human cervical cancer cells |
title | MicroRNA-150 suppresses p27(Kip1) expression and promotes cell proliferation in HeLa human cervical cancer cells |
title_full | MicroRNA-150 suppresses p27(Kip1) expression and promotes cell proliferation in HeLa human cervical cancer cells |
title_fullStr | MicroRNA-150 suppresses p27(Kip1) expression and promotes cell proliferation in HeLa human cervical cancer cells |
title_full_unstemmed | MicroRNA-150 suppresses p27(Kip1) expression and promotes cell proliferation in HeLa human cervical cancer cells |
title_short | MicroRNA-150 suppresses p27(Kip1) expression and promotes cell proliferation in HeLa human cervical cancer cells |
title_sort | microrna-150 suppresses p27(kip1) expression and promotes cell proliferation in hela human cervical cancer cells |
topic | Articles |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7491037/ https://www.ncbi.nlm.nih.gov/pubmed/32963616 http://dx.doi.org/10.3892/ol.2020.12073 |
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