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FAM83A and FAM83A-AS1 both play oncogenic roles in lung adenocarcinoma
Lung adenocarcinoma (LUAD) is the most common subtype of lung cancer. Nevertheless, the detailed molecular mechanisms of the progression of LUAD remain largely unknown. The present bioinformatics analysis reported that FAM83A and FAM83A-AS1 were upregulated in LUAD tissues and associated with progno...
Autores principales: | , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
D.A. Spandidos
2021
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7905536/ https://www.ncbi.nlm.nih.gov/pubmed/33732373 http://dx.doi.org/10.3892/ol.2021.12558 |
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author | Wang, Gaoming Li, Xiaokun Yao, Yu Jiang, Zhisheng Zhou, Hai Xie, Kai Luo, Jing Shen, Yi |
author_facet | Wang, Gaoming Li, Xiaokun Yao, Yu Jiang, Zhisheng Zhou, Hai Xie, Kai Luo, Jing Shen, Yi |
author_sort | Wang, Gaoming |
collection | PubMed |
description | Lung adenocarcinoma (LUAD) is the most common subtype of lung cancer. Nevertheless, the detailed molecular mechanisms of the progression of LUAD remain largely unknown. The present bioinformatics analysis reported that FAM83A and FAM83A-AS1 were upregulated in LUAD tissues and associated with prognosis in patients with LUAD. The purpose of the current study was to investigate the role of FAM83A and its antisense long non-coding (lnc)RNA FAM83A-AS1 in LUAD. Gene Expression Profiling Interactive Analysis was used to screen for potential oncogenes in LUAD and to analyze the clinical significance of FAM83A and FAM83A-AS1. Small interfering RNAs were constructed and transfected into LUAD cells to knock down the expression of FAM83A and FAM83A-AS1. EdU, Cell Counting Kit-8, Transwell and Matrigel assays were performed to detect the proliferation, migration and invasion of LUAD cells. The interaction between FAM83A-AS1, microRNA (miR)-495-3p and FAM83A was explored using a luciferase reporter assay. FAM83A and FAM83A-AS1 were both overexpressed in LUAD tissues compared with adjacent normal tissues. High expression of FAM83A and FAM83A-AS1 predicted worse survival and more advanced clinical stage. Knockdown of FAM83A or FAM83A-AS1 could inhibit the proliferation, migration and invasion of LUAD cells. Moreover, lncRNA FAM83A-AS1 regulated the expression of FAM83A by functioning as competing endogenous RNA for miR-495-3p. These results implicated that FAM83A and FAM83A-AS1 both played oncogenic roles in LUAD and FAM83A-AS1 could regulate the expression of FAM83A by sponging miR-495-3p. The study revealed a novel regulatory mechanism of tumor development in LUAD and FAM83A and FAM83A-AS1 may be novel biomarkers and therapeutic targets for LUAD. |
format | Online Article Text |
id | pubmed-7905536 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2021 |
publisher | D.A. Spandidos |
record_format | MEDLINE/PubMed |
spelling | pubmed-79055362021-03-16 FAM83A and FAM83A-AS1 both play oncogenic roles in lung adenocarcinoma Wang, Gaoming Li, Xiaokun Yao, Yu Jiang, Zhisheng Zhou, Hai Xie, Kai Luo, Jing Shen, Yi Oncol Lett Articles Lung adenocarcinoma (LUAD) is the most common subtype of lung cancer. Nevertheless, the detailed molecular mechanisms of the progression of LUAD remain largely unknown. The present bioinformatics analysis reported that FAM83A and FAM83A-AS1 were upregulated in LUAD tissues and associated with prognosis in patients with LUAD. The purpose of the current study was to investigate the role of FAM83A and its antisense long non-coding (lnc)RNA FAM83A-AS1 in LUAD. Gene Expression Profiling Interactive Analysis was used to screen for potential oncogenes in LUAD and to analyze the clinical significance of FAM83A and FAM83A-AS1. Small interfering RNAs were constructed and transfected into LUAD cells to knock down the expression of FAM83A and FAM83A-AS1. EdU, Cell Counting Kit-8, Transwell and Matrigel assays were performed to detect the proliferation, migration and invasion of LUAD cells. The interaction between FAM83A-AS1, microRNA (miR)-495-3p and FAM83A was explored using a luciferase reporter assay. FAM83A and FAM83A-AS1 were both overexpressed in LUAD tissues compared with adjacent normal tissues. High expression of FAM83A and FAM83A-AS1 predicted worse survival and more advanced clinical stage. Knockdown of FAM83A or FAM83A-AS1 could inhibit the proliferation, migration and invasion of LUAD cells. Moreover, lncRNA FAM83A-AS1 regulated the expression of FAM83A by functioning as competing endogenous RNA for miR-495-3p. These results implicated that FAM83A and FAM83A-AS1 both played oncogenic roles in LUAD and FAM83A-AS1 could regulate the expression of FAM83A by sponging miR-495-3p. The study revealed a novel regulatory mechanism of tumor development in LUAD and FAM83A and FAM83A-AS1 may be novel biomarkers and therapeutic targets for LUAD. D.A. Spandidos 2021-04 2021-02-17 /pmc/articles/PMC7905536/ /pubmed/33732373 http://dx.doi.org/10.3892/ol.2021.12558 Text en Copyright: © Wang 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 Wang, Gaoming Li, Xiaokun Yao, Yu Jiang, Zhisheng Zhou, Hai Xie, Kai Luo, Jing Shen, Yi FAM83A and FAM83A-AS1 both play oncogenic roles in lung adenocarcinoma |
title | FAM83A and FAM83A-AS1 both play oncogenic roles in lung adenocarcinoma |
title_full | FAM83A and FAM83A-AS1 both play oncogenic roles in lung adenocarcinoma |
title_fullStr | FAM83A and FAM83A-AS1 both play oncogenic roles in lung adenocarcinoma |
title_full_unstemmed | FAM83A and FAM83A-AS1 both play oncogenic roles in lung adenocarcinoma |
title_short | FAM83A and FAM83A-AS1 both play oncogenic roles in lung adenocarcinoma |
title_sort | fam83a and fam83a-as1 both play oncogenic roles in lung adenocarcinoma |
topic | Articles |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7905536/ https://www.ncbi.nlm.nih.gov/pubmed/33732373 http://dx.doi.org/10.3892/ol.2021.12558 |
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