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Exogenous regucalcin negatively regulates the progression of cervical adenocarcinoma
Cervical adenocarcinoma (CA) is a type of cervical cancer, and in previous decades its incidence has steadily increased. The upregulation of regucalcin (RGN) in various tumor cell types inhibits the progression of cancer. To understand the role of RGN in CA, RGN expression in human cervical cancer c...
Autores principales: | , , , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
D.A. Spandidos
2019
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6546977/ https://www.ncbi.nlm.nih.gov/pubmed/31289533 http://dx.doi.org/10.3892/ol.2019.10374 |
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author | Li, Xiaolong Huang, Yingwen Guo, Shunli Xie, Meiyu Bin, Xiaoyun Shi, Mingxia Chen, Anning Chen, Siyu Wu, Fan Hu, Qiping Zhou, Sufang |
author_facet | Li, Xiaolong Huang, Yingwen Guo, Shunli Xie, Meiyu Bin, Xiaoyun Shi, Mingxia Chen, Anning Chen, Siyu Wu, Fan Hu, Qiping Zhou, Sufang |
author_sort | Li, Xiaolong |
collection | PubMed |
description | Cervical adenocarcinoma (CA) is a type of cervical cancer, and in previous decades its incidence has steadily increased. The upregulation of regucalcin (RGN) in various tumor cell types inhibits the progression of cancer. To understand the role of RGN in CA, RGN expression in human cervical cancer compared with normal tissues was analyzed using The Cancer Genome Atlas database (TCGA). Subsequently, transfection of lentivirus-mediated RGN into HeLa cells was conducted to study its function in tumor proliferation and metastasis. The expression of RGN and proteins associated with the Wnt/β-catenin signaling pathway and epithelial-mesenchymal transition (EMT) were determined using reverse transcription-quantitative polymerase chain reaction and western blotting. Cell migration and invasion were evaluated using Transwell assays. Furthermore, cell proliferation, colony formation and cell cycle were assessed using the Cell Counting Kit-8, colony formation assay and flow cytometry, respectively. Lentivirus-mediated RGN effectively upregulated RGN expression, inhibited cell proliferation, retarded cellular invasion and promoted cell cycle arrest at the G(2)/M phase in HeLa cells. In addition, the expression levels of β-catenin, p-glycogen synthase kinase (GSK)-3β, matrix metalloproteinase (MMP)-3, MMP-7 and MMP-9 were effectively decreased, whilst those of E-cadherin and GSK-3β were increased. The results suggest that RGN may be an inhibitory factor in tumorigenesis, and its mechanism of inhibiting tumor proliferation and metastasis may be associated with Wnt/β-catenin signaling and EMT. |
format | Online Article Text |
id | pubmed-6546977 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2019 |
publisher | D.A. Spandidos |
record_format | MEDLINE/PubMed |
spelling | pubmed-65469772019-07-09 Exogenous regucalcin negatively regulates the progression of cervical adenocarcinoma Li, Xiaolong Huang, Yingwen Guo, Shunli Xie, Meiyu Bin, Xiaoyun Shi, Mingxia Chen, Anning Chen, Siyu Wu, Fan Hu, Qiping Zhou, Sufang Oncol Lett Articles Cervical adenocarcinoma (CA) is a type of cervical cancer, and in previous decades its incidence has steadily increased. The upregulation of regucalcin (RGN) in various tumor cell types inhibits the progression of cancer. To understand the role of RGN in CA, RGN expression in human cervical cancer compared with normal tissues was analyzed using The Cancer Genome Atlas database (TCGA). Subsequently, transfection of lentivirus-mediated RGN into HeLa cells was conducted to study its function in tumor proliferation and metastasis. The expression of RGN and proteins associated with the Wnt/β-catenin signaling pathway and epithelial-mesenchymal transition (EMT) were determined using reverse transcription-quantitative polymerase chain reaction and western blotting. Cell migration and invasion were evaluated using Transwell assays. Furthermore, cell proliferation, colony formation and cell cycle were assessed using the Cell Counting Kit-8, colony formation assay and flow cytometry, respectively. Lentivirus-mediated RGN effectively upregulated RGN expression, inhibited cell proliferation, retarded cellular invasion and promoted cell cycle arrest at the G(2)/M phase in HeLa cells. In addition, the expression levels of β-catenin, p-glycogen synthase kinase (GSK)-3β, matrix metalloproteinase (MMP)-3, MMP-7 and MMP-9 were effectively decreased, whilst those of E-cadherin and GSK-3β were increased. The results suggest that RGN may be an inhibitory factor in tumorigenesis, and its mechanism of inhibiting tumor proliferation and metastasis may be associated with Wnt/β-catenin signaling and EMT. D.A. Spandidos 2019-07 2019-05-20 /pmc/articles/PMC6546977/ /pubmed/31289533 http://dx.doi.org/10.3892/ol.2019.10374 Text en Copyright: © Li 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 Li, Xiaolong Huang, Yingwen Guo, Shunli Xie, Meiyu Bin, Xiaoyun Shi, Mingxia Chen, Anning Chen, Siyu Wu, Fan Hu, Qiping Zhou, Sufang Exogenous regucalcin negatively regulates the progression of cervical adenocarcinoma |
title | Exogenous regucalcin negatively regulates the progression of cervical adenocarcinoma |
title_full | Exogenous regucalcin negatively regulates the progression of cervical adenocarcinoma |
title_fullStr | Exogenous regucalcin negatively regulates the progression of cervical adenocarcinoma |
title_full_unstemmed | Exogenous regucalcin negatively regulates the progression of cervical adenocarcinoma |
title_short | Exogenous regucalcin negatively regulates the progression of cervical adenocarcinoma |
title_sort | exogenous regucalcin negatively regulates the progression of cervical adenocarcinoma |
topic | Articles |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6546977/ https://www.ncbi.nlm.nih.gov/pubmed/31289533 http://dx.doi.org/10.3892/ol.2019.10374 |
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