Cargando…
SMYD3 promotes colon adenocarcinoma (COAD) progression by mediating cell proliferation and apoptosis
Colon adenocarcinoma (COAD) is a type of common malignant tumor originating in the digestive tract. Recently, targeted therapy has had significant effects on the treatment of COAD. However, more effective molecular targets need to be developed. SET and MYND domain-containing protein 3 (SMYD3) is a t...
Autores principales: | , , , , , , |
---|---|
Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
D.A. Spandidos
2020
|
Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7472017/ https://www.ncbi.nlm.nih.gov/pubmed/32934676 http://dx.doi.org/10.3892/etm.2020.9139 |
_version_ | 1783578892477399040 |
---|---|
author | Yue, Fu-Ren Wei, Zhi-Bin Yan, Rui-Zhen Guo, Qiu-Hong Liu, Bing Zhang, Jing-Hui Li, Zheng |
author_facet | Yue, Fu-Ren Wei, Zhi-Bin Yan, Rui-Zhen Guo, Qiu-Hong Liu, Bing Zhang, Jing-Hui Li, Zheng |
author_sort | Yue, Fu-Ren |
collection | PubMed |
description | Colon adenocarcinoma (COAD) is a type of common malignant tumor originating in the digestive tract. Recently, targeted therapy has had significant effects on the treatment of COAD. However, more effective molecular targets need to be developed. SET and MYND domain-containing protein 3 (SMYD3) is a type of methyltransferase which methylates histone and non-histone proteins. The effects of SMYD3 on cancer progression and metastasis have been widely revealed. However, its possible role in COAD remains unclear. The current study demonstrated that SMYD3 expression was upregulated in human COAD tissues via analyzing the The Cancer Genome Atlas (TCGA) database and the immunohistochemical assays. Furthermore, the expression of SMYD3 was correlated with prognosis and tumor stage (P=0.038) in patients with COAD. Colony formation, MTT, FCM assays and animal assays indicated SMYD3 affected the proliferation, apoptosis and the cell cycle of COAD cells in vitro and promoted tumor growth in mice in vivo. In summary, the results demonstrated the effects of SMYD3 on COAD progression and we hypothesized that SMYD3 is a novel molecular target for COAD treatment. |
format | Online Article Text |
id | pubmed-7472017 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2020 |
publisher | D.A. Spandidos |
record_format | MEDLINE/PubMed |
spelling | pubmed-74720172020-09-14 SMYD3 promotes colon adenocarcinoma (COAD) progression by mediating cell proliferation and apoptosis Yue, Fu-Ren Wei, Zhi-Bin Yan, Rui-Zhen Guo, Qiu-Hong Liu, Bing Zhang, Jing-Hui Li, Zheng Exp Ther Med Articles Colon adenocarcinoma (COAD) is a type of common malignant tumor originating in the digestive tract. Recently, targeted therapy has had significant effects on the treatment of COAD. However, more effective molecular targets need to be developed. SET and MYND domain-containing protein 3 (SMYD3) is a type of methyltransferase which methylates histone and non-histone proteins. The effects of SMYD3 on cancer progression and metastasis have been widely revealed. However, its possible role in COAD remains unclear. The current study demonstrated that SMYD3 expression was upregulated in human COAD tissues via analyzing the The Cancer Genome Atlas (TCGA) database and the immunohistochemical assays. Furthermore, the expression of SMYD3 was correlated with prognosis and tumor stage (P=0.038) in patients with COAD. Colony formation, MTT, FCM assays and animal assays indicated SMYD3 affected the proliferation, apoptosis and the cell cycle of COAD cells in vitro and promoted tumor growth in mice in vivo. In summary, the results demonstrated the effects of SMYD3 on COAD progression and we hypothesized that SMYD3 is a novel molecular target for COAD treatment. D.A. Spandidos 2020-11 2020-08-25 /pmc/articles/PMC7472017/ /pubmed/32934676 http://dx.doi.org/10.3892/etm.2020.9139 Text en Copyright: © Yue et al. This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License (https://creativecommons.org/licenses/by-nc-nd/4.0/) , which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made. |
spellingShingle | Articles Yue, Fu-Ren Wei, Zhi-Bin Yan, Rui-Zhen Guo, Qiu-Hong Liu, Bing Zhang, Jing-Hui Li, Zheng SMYD3 promotes colon adenocarcinoma (COAD) progression by mediating cell proliferation and apoptosis |
title | SMYD3 promotes colon adenocarcinoma (COAD) progression by mediating cell proliferation and apoptosis |
title_full | SMYD3 promotes colon adenocarcinoma (COAD) progression by mediating cell proliferation and apoptosis |
title_fullStr | SMYD3 promotes colon adenocarcinoma (COAD) progression by mediating cell proliferation and apoptosis |
title_full_unstemmed | SMYD3 promotes colon adenocarcinoma (COAD) progression by mediating cell proliferation and apoptosis |
title_short | SMYD3 promotes colon adenocarcinoma (COAD) progression by mediating cell proliferation and apoptosis |
title_sort | smyd3 promotes colon adenocarcinoma (coad) progression by mediating cell proliferation and apoptosis |
topic | Articles |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7472017/ https://www.ncbi.nlm.nih.gov/pubmed/32934676 http://dx.doi.org/10.3892/etm.2020.9139 |
work_keys_str_mv | AT yuefuren smyd3promotescolonadenocarcinomacoadprogressionbymediatingcellproliferationandapoptosis AT weizhibin smyd3promotescolonadenocarcinomacoadprogressionbymediatingcellproliferationandapoptosis AT yanruizhen smyd3promotescolonadenocarcinomacoadprogressionbymediatingcellproliferationandapoptosis AT guoqiuhong smyd3promotescolonadenocarcinomacoadprogressionbymediatingcellproliferationandapoptosis AT liubing smyd3promotescolonadenocarcinomacoadprogressionbymediatingcellproliferationandapoptosis AT zhangjinghui smyd3promotescolonadenocarcinomacoadprogressionbymediatingcellproliferationandapoptosis AT lizheng smyd3promotescolonadenocarcinomacoadprogressionbymediatingcellproliferationandapoptosis |