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LncSOX4 serves an oncogenic role in the tumorigenesis of epithelial ovarian cancer by promoting cell proliferation and inhibiting apoptosis
Epithelial ovarian cancer is one of the primary causes of gynecological cancer mortality. Increasing evidence has suggested that long non-coding RNAs (lncRNAs) may serve a pivotal role in cancer development. To determine whether Lnc SRY-box 4 (SOX4), an lncRNA, promotes the self-renewal of liver tum...
Autores principales: | , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
D.A. Spandidos
2018
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Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5984009/ https://www.ncbi.nlm.nih.gov/pubmed/29693704 http://dx.doi.org/10.3892/mmr.2018.8892 |
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author | Liu, Yulan Wang, Yan Yao, Dongmei Cui, Diansheng |
author_facet | Liu, Yulan Wang, Yan Yao, Dongmei Cui, Diansheng |
author_sort | Liu, Yulan |
collection | PubMed |
description | Epithelial ovarian cancer is one of the primary causes of gynecological cancer mortality. Increasing evidence has suggested that long non-coding RNAs (lncRNAs) may serve a pivotal role in cancer development. To determine whether Lnc SRY-box 4 (SOX4), an lncRNA, promotes the self-renewal of liver tumor cells and contributes to the development of epithelial ovarian cancer, the present study investigated the expression of LncSOX4 in clinical epithelial ovarian cancer tissues and non-cancer controls by reverse transcription-quantitative polymerase chain reaction analysis. In addition, siRNA targeting LncSOX4 was designed and transfected into epithelial ovarian cancer cells to further assess the effect of knocking out LncSOX4 on cellular apoptosis, cell viability, proliferation and the cell cycle. The results demonstrated that the LncSOX4 expression level was significantly upregulated in epithelial ovarian cancer tissues (3.98 vs. 1.71, P<0.001). Silencing LncSOX4 in the SKOV3 and OVCAR3 cell lines significantly impaired cell proliferation (P<0.001). Cell cycle assays revealed that the proportion of cells in the G0/G1 phase increased significantly, whereas those in the S phase and G2/M phase decreased. Apoptosis rate additionally increased following knockdown of LncSOX4 in the two cell lines. Furthermore, it was observed that an increased LncSOX4 expression level was positively associated with larger tumor sizes, more advanced tumor grade and more distant metastases. |
format | Online Article Text |
id | pubmed-5984009 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2018 |
publisher | D.A. Spandidos |
record_format | MEDLINE/PubMed |
spelling | pubmed-59840092018-06-04 LncSOX4 serves an oncogenic role in the tumorigenesis of epithelial ovarian cancer by promoting cell proliferation and inhibiting apoptosis Liu, Yulan Wang, Yan Yao, Dongmei Cui, Diansheng Mol Med Rep Articles Epithelial ovarian cancer is one of the primary causes of gynecological cancer mortality. Increasing evidence has suggested that long non-coding RNAs (lncRNAs) may serve a pivotal role in cancer development. To determine whether Lnc SRY-box 4 (SOX4), an lncRNA, promotes the self-renewal of liver tumor cells and contributes to the development of epithelial ovarian cancer, the present study investigated the expression of LncSOX4 in clinical epithelial ovarian cancer tissues and non-cancer controls by reverse transcription-quantitative polymerase chain reaction analysis. In addition, siRNA targeting LncSOX4 was designed and transfected into epithelial ovarian cancer cells to further assess the effect of knocking out LncSOX4 on cellular apoptosis, cell viability, proliferation and the cell cycle. The results demonstrated that the LncSOX4 expression level was significantly upregulated in epithelial ovarian cancer tissues (3.98 vs. 1.71, P<0.001). Silencing LncSOX4 in the SKOV3 and OVCAR3 cell lines significantly impaired cell proliferation (P<0.001). Cell cycle assays revealed that the proportion of cells in the G0/G1 phase increased significantly, whereas those in the S phase and G2/M phase decreased. Apoptosis rate additionally increased following knockdown of LncSOX4 in the two cell lines. Furthermore, it was observed that an increased LncSOX4 expression level was positively associated with larger tumor sizes, more advanced tumor grade and more distant metastases. D.A. Spandidos 2018-06 2018-04-18 /pmc/articles/PMC5984009/ /pubmed/29693704 http://dx.doi.org/10.3892/mmr.2018.8892 Text en Copyright: © Liu 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 Liu, Yulan Wang, Yan Yao, Dongmei Cui, Diansheng LncSOX4 serves an oncogenic role in the tumorigenesis of epithelial ovarian cancer by promoting cell proliferation and inhibiting apoptosis |
title | LncSOX4 serves an oncogenic role in the tumorigenesis of epithelial ovarian cancer by promoting cell proliferation and inhibiting apoptosis |
title_full | LncSOX4 serves an oncogenic role in the tumorigenesis of epithelial ovarian cancer by promoting cell proliferation and inhibiting apoptosis |
title_fullStr | LncSOX4 serves an oncogenic role in the tumorigenesis of epithelial ovarian cancer by promoting cell proliferation and inhibiting apoptosis |
title_full_unstemmed | LncSOX4 serves an oncogenic role in the tumorigenesis of epithelial ovarian cancer by promoting cell proliferation and inhibiting apoptosis |
title_short | LncSOX4 serves an oncogenic role in the tumorigenesis of epithelial ovarian cancer by promoting cell proliferation and inhibiting apoptosis |
title_sort | lncsox4 serves an oncogenic role in the tumorigenesis of epithelial ovarian cancer by promoting cell proliferation and inhibiting apoptosis |
topic | Articles |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5984009/ https://www.ncbi.nlm.nih.gov/pubmed/29693704 http://dx.doi.org/10.3892/mmr.2018.8892 |
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