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Knockdown of lncRNA TDRG1 Inhibits Tumorigenesis in Endometrial Carcinoma Through the PI3K/AKT/mTOR Pathway
BACKGROUND AND OBJECTIVE: Endometrial carcinoma (EC) is one of the most frequently diagnosed malignancies in females. Dysregulation of lncRNA TDRG1 has been widely documented in several cancers, including EC. However, the mechanism of this lncRNA involving in EC progression remains to be further elu...
Autores principales: | , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Dove
2019
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6912007/ https://www.ncbi.nlm.nih.gov/pubmed/31849490 http://dx.doi.org/10.2147/OTT.S228168 |
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author | Sun, Ruimei Sun, Xiujiang Liu, Hua Li, Peirui |
author_facet | Sun, Ruimei Sun, Xiujiang Liu, Hua Li, Peirui |
author_sort | Sun, Ruimei |
collection | PubMed |
description | BACKGROUND AND OBJECTIVE: Endometrial carcinoma (EC) is one of the most frequently diagnosed malignancies in females. Dysregulation of lncRNA TDRG1 has been widely documented in several cancers, including EC. However, the mechanism of this lncRNA involving in EC progression remains to be further elucidated. MATERIALS AND METHODS: The enrichment levels of TDRG1 in EC tissues and cell lines were examined by RT-qPCR. Flow cytometry, cell counting kit-8 (CCK-8), transwell, and Western blot assays were conducted to assess whether TDRG1 knockdown could affect cell cycle arrest, proliferation, migration, invasion, and apoptosis of EC cells. The phosphorylation levels of mTOR, AKT and PI3K that associated with PI3K/Akt/mTOR pathway were determined by Western blot assay. RESULTS: TDRG1 expression was markedly upregulated in EC tissues and cell lines. Knockdown of TDRG1 significantly induced cell cycle arrest and apoptosis, inhibited cell proliferation, restrained the invasion and migration abilities in EC cells. Moreover, TDRG1 silencing decreased the protein levels of p-AKT, p-PI3K, and p-mTOR of EC cells. CONCLUSION: Our data underlined the implication of TDRG1 in EC progression, proposing that targeting TDRG1 might be a potential therapeutic avenue in EC. |
format | Online Article Text |
id | pubmed-6912007 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2019 |
publisher | Dove |
record_format | MEDLINE/PubMed |
spelling | pubmed-69120072019-12-17 Knockdown of lncRNA TDRG1 Inhibits Tumorigenesis in Endometrial Carcinoma Through the PI3K/AKT/mTOR Pathway Sun, Ruimei Sun, Xiujiang Liu, Hua Li, Peirui Onco Targets Ther Original Research BACKGROUND AND OBJECTIVE: Endometrial carcinoma (EC) is one of the most frequently diagnosed malignancies in females. Dysregulation of lncRNA TDRG1 has been widely documented in several cancers, including EC. However, the mechanism of this lncRNA involving in EC progression remains to be further elucidated. MATERIALS AND METHODS: The enrichment levels of TDRG1 in EC tissues and cell lines were examined by RT-qPCR. Flow cytometry, cell counting kit-8 (CCK-8), transwell, and Western blot assays were conducted to assess whether TDRG1 knockdown could affect cell cycle arrest, proliferation, migration, invasion, and apoptosis of EC cells. The phosphorylation levels of mTOR, AKT and PI3K that associated with PI3K/Akt/mTOR pathway were determined by Western blot assay. RESULTS: TDRG1 expression was markedly upregulated in EC tissues and cell lines. Knockdown of TDRG1 significantly induced cell cycle arrest and apoptosis, inhibited cell proliferation, restrained the invasion and migration abilities in EC cells. Moreover, TDRG1 silencing decreased the protein levels of p-AKT, p-PI3K, and p-mTOR of EC cells. CONCLUSION: Our data underlined the implication of TDRG1 in EC progression, proposing that targeting TDRG1 might be a potential therapeutic avenue in EC. Dove 2019-12-11 /pmc/articles/PMC6912007/ /pubmed/31849490 http://dx.doi.org/10.2147/OTT.S228168 Text en © 2019 Sun et al. http://creativecommons.org/licenses/by-nc/3.0/ This work is published and licensed by Dove Medical Press Limited. The full terms of this license are available at https://www.dovepress.com/terms.php and incorporate the Creative Commons Attribution – Non Commercial (unported, v3.0) License (http://creativecommons.org/licenses/by-nc/3.0/). By accessing the work you hereby accept the Terms. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed. For permission for commercial use of this work, please see paragraphs 4.2 and 5 of our Terms (https://www.dovepress.com/terms.php). |
spellingShingle | Original Research Sun, Ruimei Sun, Xiujiang Liu, Hua Li, Peirui Knockdown of lncRNA TDRG1 Inhibits Tumorigenesis in Endometrial Carcinoma Through the PI3K/AKT/mTOR Pathway |
title | Knockdown of lncRNA TDRG1 Inhibits Tumorigenesis in Endometrial Carcinoma Through the PI3K/AKT/mTOR Pathway |
title_full | Knockdown of lncRNA TDRG1 Inhibits Tumorigenesis in Endometrial Carcinoma Through the PI3K/AKT/mTOR Pathway |
title_fullStr | Knockdown of lncRNA TDRG1 Inhibits Tumorigenesis in Endometrial Carcinoma Through the PI3K/AKT/mTOR Pathway |
title_full_unstemmed | Knockdown of lncRNA TDRG1 Inhibits Tumorigenesis in Endometrial Carcinoma Through the PI3K/AKT/mTOR Pathway |
title_short | Knockdown of lncRNA TDRG1 Inhibits Tumorigenesis in Endometrial Carcinoma Through the PI3K/AKT/mTOR Pathway |
title_sort | knockdown of lncrna tdrg1 inhibits tumorigenesis in endometrial carcinoma through the pi3k/akt/mtor pathway |
topic | Original Research |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6912007/ https://www.ncbi.nlm.nih.gov/pubmed/31849490 http://dx.doi.org/10.2147/OTT.S228168 |
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