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miR-552 promotes ovarian cancer progression by regulating PTEN pathway
BACKGROUND: Increasing researches have demonstrated the critical functions of MicroRNAs (miRNAs) in the progression of malignant tumors, including ovarian cancer. It was reported that miR-552 was an important oncogene in both breast cancer and colorectal cancer. However, the role of miR-552 in ovari...
Autores principales: | , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
BioMed Central
2019
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6900846/ https://www.ncbi.nlm.nih.gov/pubmed/31815639 http://dx.doi.org/10.1186/s13048-019-0589-y |
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author | Zhao, Wenman Han, Tao Li, Bao Ma, Qianyun Yang, Pinghua Li, Hengyu |
author_facet | Zhao, Wenman Han, Tao Li, Bao Ma, Qianyun Yang, Pinghua Li, Hengyu |
author_sort | Zhao, Wenman |
collection | PubMed |
description | BACKGROUND: Increasing researches have demonstrated the critical functions of MicroRNAs (miRNAs) in the progression of malignant tumors, including ovarian cancer. It was reported that miR-552 was an important oncogene in both breast cancer and colorectal cancer. However, the role of miR-552 in ovarian cancer (OC) remains to be elucidated. METHODS: RT-PCR and western blot analysis were used to detect the expression of miR-552 and PTEN. The impact of miR-552 on ovarian cancer proliferation and metastasis was investigated in vitro. The prognostic value of miR-552 was evaluated using the online bioinformatics tool Kaplan-Meier plotter. RESULTS: In the present study, we for first found that miR-552 was upregulated in ovarian cancer, especially in metastatic and recurrence ovarian cancer. Forced miR-552 expression promotes the growth and metastasis of ovarian cancer cells. Consistently, miR-552 interference inhibits the proliferation and metastasis of ovarian cancer cells. Mechanically, bioinformatics and luciferase reporter analysis identified Phosphatase and tension homolog (PTEN) as a direct target of miR-552. miR-552 downregulated the PTEN mRNA and protein expression in ovarian cancer cells. Furthermore, the PTEN siRNA abolishes the discrepancy of growth and metastasis capacity between miR-552 mimic ovarian cells and control cells. More importantly, upregulation of miR-552 predicts the poor prognosis of ovarian cancer patients. CONCLUSION: Our findings revealed that miR-552 could promote ovarian cancer cells progression by targeting PTEN signaling and might therefore be useful to predict patient prognosis. |
format | Online Article Text |
id | pubmed-6900846 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2019 |
publisher | BioMed Central |
record_format | MEDLINE/PubMed |
spelling | pubmed-69008462019-12-11 miR-552 promotes ovarian cancer progression by regulating PTEN pathway Zhao, Wenman Han, Tao Li, Bao Ma, Qianyun Yang, Pinghua Li, Hengyu J Ovarian Res Research BACKGROUND: Increasing researches have demonstrated the critical functions of MicroRNAs (miRNAs) in the progression of malignant tumors, including ovarian cancer. It was reported that miR-552 was an important oncogene in both breast cancer and colorectal cancer. However, the role of miR-552 in ovarian cancer (OC) remains to be elucidated. METHODS: RT-PCR and western blot analysis were used to detect the expression of miR-552 and PTEN. The impact of miR-552 on ovarian cancer proliferation and metastasis was investigated in vitro. The prognostic value of miR-552 was evaluated using the online bioinformatics tool Kaplan-Meier plotter. RESULTS: In the present study, we for first found that miR-552 was upregulated in ovarian cancer, especially in metastatic and recurrence ovarian cancer. Forced miR-552 expression promotes the growth and metastasis of ovarian cancer cells. Consistently, miR-552 interference inhibits the proliferation and metastasis of ovarian cancer cells. Mechanically, bioinformatics and luciferase reporter analysis identified Phosphatase and tension homolog (PTEN) as a direct target of miR-552. miR-552 downregulated the PTEN mRNA and protein expression in ovarian cancer cells. Furthermore, the PTEN siRNA abolishes the discrepancy of growth and metastasis capacity between miR-552 mimic ovarian cells and control cells. More importantly, upregulation of miR-552 predicts the poor prognosis of ovarian cancer patients. CONCLUSION: Our findings revealed that miR-552 could promote ovarian cancer cells progression by targeting PTEN signaling and might therefore be useful to predict patient prognosis. BioMed Central 2019-12-09 /pmc/articles/PMC6900846/ /pubmed/31815639 http://dx.doi.org/10.1186/s13048-019-0589-y Text en © The Author(s). 2019 Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated. |
spellingShingle | Research Zhao, Wenman Han, Tao Li, Bao Ma, Qianyun Yang, Pinghua Li, Hengyu miR-552 promotes ovarian cancer progression by regulating PTEN pathway |
title | miR-552 promotes ovarian cancer progression by regulating PTEN pathway |
title_full | miR-552 promotes ovarian cancer progression by regulating PTEN pathway |
title_fullStr | miR-552 promotes ovarian cancer progression by regulating PTEN pathway |
title_full_unstemmed | miR-552 promotes ovarian cancer progression by regulating PTEN pathway |
title_short | miR-552 promotes ovarian cancer progression by regulating PTEN pathway |
title_sort | mir-552 promotes ovarian cancer progression by regulating pten pathway |
topic | Research |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6900846/ https://www.ncbi.nlm.nih.gov/pubmed/31815639 http://dx.doi.org/10.1186/s13048-019-0589-y |
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