Cargando…
TRIM27 promotes the development of esophagus cancer via regulating PTEN/AKT signaling pathway
BACKGROUND: Tripartite motif‑containing 27 (TRIM27) belongs to the TRIM protein family, which is closely related to the progression of some certain human cancers. Nevertheless, the biological function of TRIM27 in esophageal squamous cell carcinoma (ESCC) is still not clear. The aim of present resea...
Autores principales: | , , , |
---|---|
Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
BioMed Central
2019
|
Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6839104/ https://www.ncbi.nlm.nih.gov/pubmed/31719796 http://dx.doi.org/10.1186/s12935-019-0998-4 |
_version_ | 1783467343376023552 |
---|---|
author | Ma, Liang Yao, Ninghua Chen, Ping Zhuang, Zhixiang |
author_facet | Ma, Liang Yao, Ninghua Chen, Ping Zhuang, Zhixiang |
author_sort | Ma, Liang |
collection | PubMed |
description | BACKGROUND: Tripartite motif‑containing 27 (TRIM27) belongs to the TRIM protein family, which is closely related to the progression of some certain human cancers. Nevertheless, the biological function of TRIM27 in esophageal squamous cell carcinoma (ESCC) is still not clear. The aim of present research is to examine the function of TRIM27 in ESCC cells. METHODS: In the present study, RNA interference (RNAi) and lentiviral vector were used to knockdown and overexpression of TRIM27 in ESCC cells respectively. qRT-PCR and western blot were used to examine the expression of TRIM27 in ESCC cells. Cell counting kit-8 (CCK-8) assay was performed to determine the proliferation of cells. RESULTS: Our analyses indicated that TRIM27 was a pro-proliferation factor in ESCC cells. Moreover, overexpression of TRIM27 deeply suppressed the apoptosis of ESCC cells and accelerated its glucose uptake. In addition, an AKT inhibitor LY294002 was used to determine the connection between TRIM27 and AKT in ESCC cells. Our results demonstrated that TRIM27 has involved in the PI3/AKT signaling pathway. Moreover, TRIM27 interacted with PTEN and mediated its poly-ubiquitination in ESCC cells. Importantly, the glycolysis inhibitor 3-BrPA also inhibited the effect of TRIM27 on ESCC cells. Hence, TRIM27 also participated in the regulation of energy metabolism in ESCC cells. CONCLUSIONS: This research not only gained a deep insight into the biological function of TRIM27 but also elucidated its potential target and signaling pathway in human ESCC cells. |
format | Online Article Text |
id | pubmed-6839104 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2019 |
publisher | BioMed Central |
record_format | MEDLINE/PubMed |
spelling | pubmed-68391042019-11-12 TRIM27 promotes the development of esophagus cancer via regulating PTEN/AKT signaling pathway Ma, Liang Yao, Ninghua Chen, Ping Zhuang, Zhixiang Cancer Cell Int Primary Research BACKGROUND: Tripartite motif‑containing 27 (TRIM27) belongs to the TRIM protein family, which is closely related to the progression of some certain human cancers. Nevertheless, the biological function of TRIM27 in esophageal squamous cell carcinoma (ESCC) is still not clear. The aim of present research is to examine the function of TRIM27 in ESCC cells. METHODS: In the present study, RNA interference (RNAi) and lentiviral vector were used to knockdown and overexpression of TRIM27 in ESCC cells respectively. qRT-PCR and western blot were used to examine the expression of TRIM27 in ESCC cells. Cell counting kit-8 (CCK-8) assay was performed to determine the proliferation of cells. RESULTS: Our analyses indicated that TRIM27 was a pro-proliferation factor in ESCC cells. Moreover, overexpression of TRIM27 deeply suppressed the apoptosis of ESCC cells and accelerated its glucose uptake. In addition, an AKT inhibitor LY294002 was used to determine the connection between TRIM27 and AKT in ESCC cells. Our results demonstrated that TRIM27 has involved in the PI3/AKT signaling pathway. Moreover, TRIM27 interacted with PTEN and mediated its poly-ubiquitination in ESCC cells. Importantly, the glycolysis inhibitor 3-BrPA also inhibited the effect of TRIM27 on ESCC cells. Hence, TRIM27 also participated in the regulation of energy metabolism in ESCC cells. CONCLUSIONS: This research not only gained a deep insight into the biological function of TRIM27 but also elucidated its potential target and signaling pathway in human ESCC cells. BioMed Central 2019-11-08 /pmc/articles/PMC6839104/ /pubmed/31719796 http://dx.doi.org/10.1186/s12935-019-0998-4 Text en © The Author(s) 2019 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 Ma, Liang Yao, Ninghua Chen, Ping Zhuang, Zhixiang TRIM27 promotes the development of esophagus cancer via regulating PTEN/AKT signaling pathway |
title | TRIM27 promotes the development of esophagus cancer via regulating PTEN/AKT signaling pathway |
title_full | TRIM27 promotes the development of esophagus cancer via regulating PTEN/AKT signaling pathway |
title_fullStr | TRIM27 promotes the development of esophagus cancer via regulating PTEN/AKT signaling pathway |
title_full_unstemmed | TRIM27 promotes the development of esophagus cancer via regulating PTEN/AKT signaling pathway |
title_short | TRIM27 promotes the development of esophagus cancer via regulating PTEN/AKT signaling pathway |
title_sort | trim27 promotes the development of esophagus cancer via regulating pten/akt signaling pathway |
topic | Primary Research |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6839104/ https://www.ncbi.nlm.nih.gov/pubmed/31719796 http://dx.doi.org/10.1186/s12935-019-0998-4 |
work_keys_str_mv | AT maliang trim27promotesthedevelopmentofesophaguscancerviaregulatingptenaktsignalingpathway AT yaoninghua trim27promotesthedevelopmentofesophaguscancerviaregulatingptenaktsignalingpathway AT chenping trim27promotesthedevelopmentofesophaguscancerviaregulatingptenaktsignalingpathway AT zhuangzhixiang trim27promotesthedevelopmentofesophaguscancerviaregulatingptenaktsignalingpathway |