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LncRNA EGOT decreases breast cancer cell viability and migration via inactivation of the Hedgehog pathway
The long noncoding RNA (lncRNA) Eosinophil Granule Ontogeny Transcript (EGOT) has been reported to inhibit the proliferation and migration of glioma cells, and promote the development and progression of gastric cancer through the Hedgehog (Hh) signaling pathway. This study was conducted to assess th...
Autores principales: | , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
John Wiley and Sons Inc.
2020
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7193175/ https://www.ncbi.nlm.nih.gov/pubmed/32150666 http://dx.doi.org/10.1002/2211-5463.12833 |
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author | Qiu, Shuang Chen, Guobing Peng, Juan Liu, Jia Chen, Jumin Wang, Jianjun Li, Li Yang, Kunxian |
author_facet | Qiu, Shuang Chen, Guobing Peng, Juan Liu, Jia Chen, Jumin Wang, Jianjun Li, Li Yang, Kunxian |
author_sort | Qiu, Shuang |
collection | PubMed |
description | The long noncoding RNA (lncRNA) Eosinophil Granule Ontogeny Transcript (EGOT) has been reported to inhibit the proliferation and migration of glioma cells, and promote the development and progression of gastric cancer through the Hedgehog (Hh) signaling pathway. This study was conducted to assess the role of EGOT in the progression of breast cancer. We observed that EGOT is significantly down‐regulated in breast cancer tissues and cell lines, and EGOT expression is negatively correlated with the Ki67 expression. Overexpression of EGOT in BT549 cells decreased cell viability and migration. In addition, overexpression of EGOT resulted in decreases in expression of key genes in the Hh pathway, including Gli1, smoothened protein, protein patched homolog 1 and Hedgehog‐interacting protein (HHIP). Breast cancer tissues exhibited an increase in Gli1 expressions. Altered expression of Gli1, smoothened protein, protein patched homolog 1 and HHIP caused by EGOT overexpression were fully restored in cells transfected with plasmid complementory DNA (pcDNA) EGOT and treated with purmorphamine, an agonist of the Hh pathway. Cell viability and migration were also restored by purmorphamine. We conclude that lncRNA EGOT may inhibit breast cancer cell viability and migration via inactivation of the Hh pathway. |
format | Online Article Text |
id | pubmed-7193175 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2020 |
publisher | John Wiley and Sons Inc. |
record_format | MEDLINE/PubMed |
spelling | pubmed-71931752020-05-01 LncRNA EGOT decreases breast cancer cell viability and migration via inactivation of the Hedgehog pathway Qiu, Shuang Chen, Guobing Peng, Juan Liu, Jia Chen, Jumin Wang, Jianjun Li, Li Yang, Kunxian FEBS Open Bio Research Articles The long noncoding RNA (lncRNA) Eosinophil Granule Ontogeny Transcript (EGOT) has been reported to inhibit the proliferation and migration of glioma cells, and promote the development and progression of gastric cancer through the Hedgehog (Hh) signaling pathway. This study was conducted to assess the role of EGOT in the progression of breast cancer. We observed that EGOT is significantly down‐regulated in breast cancer tissues and cell lines, and EGOT expression is negatively correlated with the Ki67 expression. Overexpression of EGOT in BT549 cells decreased cell viability and migration. In addition, overexpression of EGOT resulted in decreases in expression of key genes in the Hh pathway, including Gli1, smoothened protein, protein patched homolog 1 and Hedgehog‐interacting protein (HHIP). Breast cancer tissues exhibited an increase in Gli1 expressions. Altered expression of Gli1, smoothened protein, protein patched homolog 1 and HHIP caused by EGOT overexpression were fully restored in cells transfected with plasmid complementory DNA (pcDNA) EGOT and treated with purmorphamine, an agonist of the Hh pathway. Cell viability and migration were also restored by purmorphamine. We conclude that lncRNA EGOT may inhibit breast cancer cell viability and migration via inactivation of the Hh pathway. John Wiley and Sons Inc. 2020-04-08 /pmc/articles/PMC7193175/ /pubmed/32150666 http://dx.doi.org/10.1002/2211-5463.12833 Text en © 2020 The Authors. Published by FEBS Press and John Wiley & Sons Ltd. This is an open access article under the terms of the http://creativecommons.org/licenses/by/4.0/ License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Research Articles Qiu, Shuang Chen, Guobing Peng, Juan Liu, Jia Chen, Jumin Wang, Jianjun Li, Li Yang, Kunxian LncRNA EGOT decreases breast cancer cell viability and migration via inactivation of the Hedgehog pathway |
title | LncRNA EGOT decreases breast cancer cell viability and migration via inactivation of the Hedgehog pathway |
title_full | LncRNA EGOT decreases breast cancer cell viability and migration via inactivation of the Hedgehog pathway |
title_fullStr | LncRNA EGOT decreases breast cancer cell viability and migration via inactivation of the Hedgehog pathway |
title_full_unstemmed | LncRNA EGOT decreases breast cancer cell viability and migration via inactivation of the Hedgehog pathway |
title_short | LncRNA EGOT decreases breast cancer cell viability and migration via inactivation of the Hedgehog pathway |
title_sort | lncrna egot decreases breast cancer cell viability and migration via inactivation of the hedgehog pathway |
topic | Research Articles |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7193175/ https://www.ncbi.nlm.nih.gov/pubmed/32150666 http://dx.doi.org/10.1002/2211-5463.12833 |
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