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Contribution of KCTD12 to esophageal squamous cell carcinoma
BACKGROUND: It has been shown that the expression of potassium channel tetramerization domain containing 12 (KCTD12) as a regulator of GABAB receptor signaling is reversely associated with gastrointestinal stromal tumors. In present study we examined the probable role of KCTD12 in regulation of seve...
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/PMC6114029/ https://www.ncbi.nlm.nih.gov/pubmed/30157793 http://dx.doi.org/10.1186/s12885-018-4765-z |
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author | Abbaszadegan, Mohammad Reza Taghehchian, Negin Li, Liping Aarabi, Azadeh Moghbeli, Meysam |
author_facet | Abbaszadegan, Mohammad Reza Taghehchian, Negin Li, Liping Aarabi, Azadeh Moghbeli, Meysam |
author_sort | Abbaszadegan, Mohammad Reza |
collection | PubMed |
description | BACKGROUND: It has been shown that the expression of potassium channel tetramerization domain containing 12 (KCTD12) as a regulator of GABAB receptor signaling is reversely associated with gastrointestinal stromal tumors. In present study we examined the probable role of KCTD12 in regulation of several signaling pathways and chromatin remodelers in esophageal squamous cell carcinoma (ESCC). METHODS: KCTD12 ectopic expression was done in KYSE30 cell line. Comparative quantitative real time PCR was used to assess the expression of stem cell factors and several factors belonging to the WNT/NOTCH and chromatin remodeling in transfected cells in comparison with non-transfected cells. RESULTS: We observed that the KCTD12 significantly down regulated expression of NANOG, SOX2, SALL4, KLF4, MAML1, PYGO2, BMI1, BRG1, MSI1, MEIS1, EGFR, DIDO1, ABCC4, ABCG2, and CRIPTO1 in transfected cells in comparison with non-transfected cells. Migration assay showed a significant decrease in cell movement in ectopic expressed cells in comparison with non-transfected cells (p = 0.02). Moreover, KCTD12 significantly decreased the 5FU resistance in transfected cells (p = 0.01). CONCLUSIONS: KCTD12 may exert its inhibitory role in ESCC through the suppression of WNT /NOTCH, stem cell factors, and chromatin remodelers and can be introduced as an efficient therapeutic marker. |
format | Online Article Text |
id | pubmed-6114029 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2018 |
publisher | BioMed Central |
record_format | MEDLINE/PubMed |
spelling | pubmed-61140292018-09-04 Contribution of KCTD12 to esophageal squamous cell carcinoma Abbaszadegan, Mohammad Reza Taghehchian, Negin Li, Liping Aarabi, Azadeh Moghbeli, Meysam BMC Cancer Research Article BACKGROUND: It has been shown that the expression of potassium channel tetramerization domain containing 12 (KCTD12) as a regulator of GABAB receptor signaling is reversely associated with gastrointestinal stromal tumors. In present study we examined the probable role of KCTD12 in regulation of several signaling pathways and chromatin remodelers in esophageal squamous cell carcinoma (ESCC). METHODS: KCTD12 ectopic expression was done in KYSE30 cell line. Comparative quantitative real time PCR was used to assess the expression of stem cell factors and several factors belonging to the WNT/NOTCH and chromatin remodeling in transfected cells in comparison with non-transfected cells. RESULTS: We observed that the KCTD12 significantly down regulated expression of NANOG, SOX2, SALL4, KLF4, MAML1, PYGO2, BMI1, BRG1, MSI1, MEIS1, EGFR, DIDO1, ABCC4, ABCG2, and CRIPTO1 in transfected cells in comparison with non-transfected cells. Migration assay showed a significant decrease in cell movement in ectopic expressed cells in comparison with non-transfected cells (p = 0.02). Moreover, KCTD12 significantly decreased the 5FU resistance in transfected cells (p = 0.01). CONCLUSIONS: KCTD12 may exert its inhibitory role in ESCC through the suppression of WNT /NOTCH, stem cell factors, and chromatin remodelers and can be introduced as an efficient therapeutic marker. BioMed Central 2018-08-29 /pmc/articles/PMC6114029/ /pubmed/30157793 http://dx.doi.org/10.1186/s12885-018-4765-z 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 | Research Article Abbaszadegan, Mohammad Reza Taghehchian, Negin Li, Liping Aarabi, Azadeh Moghbeli, Meysam Contribution of KCTD12 to esophageal squamous cell carcinoma |
title | Contribution of KCTD12 to esophageal squamous cell carcinoma |
title_full | Contribution of KCTD12 to esophageal squamous cell carcinoma |
title_fullStr | Contribution of KCTD12 to esophageal squamous cell carcinoma |
title_full_unstemmed | Contribution of KCTD12 to esophageal squamous cell carcinoma |
title_short | Contribution of KCTD12 to esophageal squamous cell carcinoma |
title_sort | contribution of kctd12 to esophageal squamous cell carcinoma |
topic | Research Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6114029/ https://www.ncbi.nlm.nih.gov/pubmed/30157793 http://dx.doi.org/10.1186/s12885-018-4765-z |
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