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Silencing of Synuclein-γ inhibits human cervical cancer through the AKT signaling pathway
BACKGROUND: Synuclein-γ has been demonstrated to be highly expressed in various human cancers including cervical cancer, and has been shown to play a critical role in tumor aggressiveness. We aimed to investigate the role of Synuclein-γ in human cervical cancer in vitro and in vivo. METHOD: Reverse...
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/PMC6617888/ https://www.ncbi.nlm.nih.gov/pubmed/31333726 http://dx.doi.org/10.1186/s11658-019-0172-y |
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author | Zhang, Chunnian Gu, Liqin Li, Xiafang Wang, Jianzhong |
author_facet | Zhang, Chunnian Gu, Liqin Li, Xiafang Wang, Jianzhong |
author_sort | Zhang, Chunnian |
collection | PubMed |
description | BACKGROUND: Synuclein-γ has been demonstrated to be highly expressed in various human cancers including cervical cancer, and has been shown to play a critical role in tumor aggressiveness. We aimed to investigate the role of Synuclein-γ in human cervical cancer in vitro and in vivo. METHOD: Reverse transcription-quantitative polymerase chain reaction assay and Western blot assay were used to detect the mRNA and protein expression, respectively. 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay and colony formation assay were performed to measure the viabilities of cancer cells. Flow cytometry assay was used to detect the cell cycle and apoptosis. Moreover, an animal experiment was performed to evaluate the biological behavior of Synuclein-γ in vivo. RESULTS: In the current study, we found that Synuclein-γ was obviously over-expressed in cervical cancer tissues compared to the adjacent non-cancer tissues. Cervical cancer cells transfected with Synuclein-γ siRNA demonstrated significant inhibition of cancer proliferation (P < 0.01), cell cycle arrest at G0/G1 phase, and cell apoptosis (P < 0.05). Moreover, down-regulation of Synuclein-γ significantly inhibited cervical cancer growth in vivo. In addition, protein levels of AKT, c-Myc and Cyclin D1 were much lower in the Synuclein-γ siRNA-treated groups than that in the control group. CONCLUSIONS: Synuclein-γ inhibition reduced cervical cancer tumor growth through the AKT pathway. This effect represented a therapeutic opportunity and provided a novel target for cervical cancer treatment. |
format | Online Article Text |
id | pubmed-6617888 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2019 |
publisher | BioMed Central |
record_format | MEDLINE/PubMed |
spelling | pubmed-66178882019-07-22 Silencing of Synuclein-γ inhibits human cervical cancer through the AKT signaling pathway Zhang, Chunnian Gu, Liqin Li, Xiafang Wang, Jianzhong Cell Mol Biol Lett Research Letter BACKGROUND: Synuclein-γ has been demonstrated to be highly expressed in various human cancers including cervical cancer, and has been shown to play a critical role in tumor aggressiveness. We aimed to investigate the role of Synuclein-γ in human cervical cancer in vitro and in vivo. METHOD: Reverse transcription-quantitative polymerase chain reaction assay and Western blot assay were used to detect the mRNA and protein expression, respectively. 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay and colony formation assay were performed to measure the viabilities of cancer cells. Flow cytometry assay was used to detect the cell cycle and apoptosis. Moreover, an animal experiment was performed to evaluate the biological behavior of Synuclein-γ in vivo. RESULTS: In the current study, we found that Synuclein-γ was obviously over-expressed in cervical cancer tissues compared to the adjacent non-cancer tissues. Cervical cancer cells transfected with Synuclein-γ siRNA demonstrated significant inhibition of cancer proliferation (P < 0.01), cell cycle arrest at G0/G1 phase, and cell apoptosis (P < 0.05). Moreover, down-regulation of Synuclein-γ significantly inhibited cervical cancer growth in vivo. In addition, protein levels of AKT, c-Myc and Cyclin D1 were much lower in the Synuclein-γ siRNA-treated groups than that in the control group. CONCLUSIONS: Synuclein-γ inhibition reduced cervical cancer tumor growth through the AKT pathway. This effect represented a therapeutic opportunity and provided a novel target for cervical cancer treatment. BioMed Central 2019-07-10 /pmc/articles/PMC6617888/ /pubmed/31333726 http://dx.doi.org/10.1186/s11658-019-0172-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 Letter Zhang, Chunnian Gu, Liqin Li, Xiafang Wang, Jianzhong Silencing of Synuclein-γ inhibits human cervical cancer through the AKT signaling pathway |
title | Silencing of Synuclein-γ inhibits human cervical cancer through the AKT signaling pathway |
title_full | Silencing of Synuclein-γ inhibits human cervical cancer through the AKT signaling pathway |
title_fullStr | Silencing of Synuclein-γ inhibits human cervical cancer through the AKT signaling pathway |
title_full_unstemmed | Silencing of Synuclein-γ inhibits human cervical cancer through the AKT signaling pathway |
title_short | Silencing of Synuclein-γ inhibits human cervical cancer through the AKT signaling pathway |
title_sort | silencing of synuclein-γ inhibits human cervical cancer through the akt signaling pathway |
topic | Research Letter |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6617888/ https://www.ncbi.nlm.nih.gov/pubmed/31333726 http://dx.doi.org/10.1186/s11658-019-0172-y |
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