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SOX2OT knockdown derived changes in mitotic regulatory gene network of cancer cells
BACKGROUND: SOX2 overlapping transcript (SOX2OT) is a long non-coding RNA, over-expressed in human tumor tissues and embryonic cells. Evidences support its function in the cell cycle; however there is no clear mechanism explaining its function in cell proliferation regulation. Here we investigated c...
Autores principales: | , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
BioMed Central
2018
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6126007/ https://www.ncbi.nlm.nih.gov/pubmed/30202240 http://dx.doi.org/10.1186/s12935-018-0618-8 |
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author | Saghaeian Jazi, Marie Samaei, Nader Mansour Mowla, Seyed Javad Arefnezhad, Babak Kouhsar, Morteza |
author_facet | Saghaeian Jazi, Marie Samaei, Nader Mansour Mowla, Seyed Javad Arefnezhad, Babak Kouhsar, Morteza |
author_sort | Saghaeian Jazi, Marie |
collection | PubMed |
description | BACKGROUND: SOX2 overlapping transcript (SOX2OT) is a long non-coding RNA, over-expressed in human tumor tissues and embryonic cells. Evidences support its function in the cell cycle; however there is no clear mechanism explaining its function in cell proliferation regulation. Here we investigated cancer cell response to SOX2OT knockdown by RNA sequencing. METHODS: SOX2OT expression was inhibited by siRNA in two cancer cell lines (A549, U-87 MG), then the RNA of treated cells were used for the cDNA library synthesis and RNA sequencing. The differentially expressed genes were used for functional enrichment and the gene expression network was analyzed to find the most relevant biological process with SOX2OT function. Furthermore, the expression change of candidate genes was measured by qRT-PCR for more confirmation and the cell cycle was monitored by PI staining. RESULTS: Our findings showed that SOX2OT knockdown affects the cellular gene expression generally with enriched cell proliferation and development biological process. Particularly, the cell cycle and mitotic regulatory genes expression including: CDK2, CDK2AP2, ACTR3, and chromosome structure associated genes like SMC4, INCENP and GNL3L are changed in treated cancer cells. CONCLUSION: Our results propound SOX2OT association with cell cycle and mitosis regulation in cancer cells. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (10.1186/s12935-018-0618-8) contains supplementary material, which is available to authorized users. |
format | Online Article Text |
id | pubmed-6126007 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2018 |
publisher | BioMed Central |
record_format | MEDLINE/PubMed |
spelling | pubmed-61260072018-09-10 SOX2OT knockdown derived changes in mitotic regulatory gene network of cancer cells Saghaeian Jazi, Marie Samaei, Nader Mansour Mowla, Seyed Javad Arefnezhad, Babak Kouhsar, Morteza Cancer Cell Int Primary Research BACKGROUND: SOX2 overlapping transcript (SOX2OT) is a long non-coding RNA, over-expressed in human tumor tissues and embryonic cells. Evidences support its function in the cell cycle; however there is no clear mechanism explaining its function in cell proliferation regulation. Here we investigated cancer cell response to SOX2OT knockdown by RNA sequencing. METHODS: SOX2OT expression was inhibited by siRNA in two cancer cell lines (A549, U-87 MG), then the RNA of treated cells were used for the cDNA library synthesis and RNA sequencing. The differentially expressed genes were used for functional enrichment and the gene expression network was analyzed to find the most relevant biological process with SOX2OT function. Furthermore, the expression change of candidate genes was measured by qRT-PCR for more confirmation and the cell cycle was monitored by PI staining. RESULTS: Our findings showed that SOX2OT knockdown affects the cellular gene expression generally with enriched cell proliferation and development biological process. Particularly, the cell cycle and mitotic regulatory genes expression including: CDK2, CDK2AP2, ACTR3, and chromosome structure associated genes like SMC4, INCENP and GNL3L are changed in treated cancer cells. CONCLUSION: Our results propound SOX2OT association with cell cycle and mitosis regulation in cancer cells. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (10.1186/s12935-018-0618-8) contains supplementary material, which is available to authorized users. BioMed Central 2018-09-05 /pmc/articles/PMC6126007/ /pubmed/30202240 http://dx.doi.org/10.1186/s12935-018-0618-8 Text en © The Author(s) 2018 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 | Primary Research Saghaeian Jazi, Marie Samaei, Nader Mansour Mowla, Seyed Javad Arefnezhad, Babak Kouhsar, Morteza SOX2OT knockdown derived changes in mitotic regulatory gene network of cancer cells |
title | SOX2OT knockdown derived changes in mitotic regulatory gene network of cancer cells |
title_full | SOX2OT knockdown derived changes in mitotic regulatory gene network of cancer cells |
title_fullStr | SOX2OT knockdown derived changes in mitotic regulatory gene network of cancer cells |
title_full_unstemmed | SOX2OT knockdown derived changes in mitotic regulatory gene network of cancer cells |
title_short | SOX2OT knockdown derived changes in mitotic regulatory gene network of cancer cells |
title_sort | sox2ot knockdown derived changes in mitotic regulatory gene network of cancer cells |
topic | Primary Research |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6126007/ https://www.ncbi.nlm.nih.gov/pubmed/30202240 http://dx.doi.org/10.1186/s12935-018-0618-8 |
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