Cargando…

The comprehensive investigation of transcription factor AP-2 alpha in lung adenocarcinoma

BACKGROUND: Transcription factor AP-2 alpha (TFAP2A) has been reported to participate in various tumors. However, the transcriptional levels and prognostic values of TFAP2A remain elusive in lung adenocarcinoma (LUAD). The purpose of the present study was to investigate the impact of the TFAP2A in L...

Descripción completa

Detalles Bibliográficos
Autores principales: Liao, Hongli, Lin, Peng
Formato: Online Artículo Texto
Lenguaje:English
Publicado: AME Publishing Company 2020
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8799082/
https://www.ncbi.nlm.nih.gov/pubmed/35117502
http://dx.doi.org/10.21037/tcr.2020.01.58
_version_ 1784641982387191808
author Liao, Hongli
Lin, Peng
author_facet Liao, Hongli
Lin, Peng
author_sort Liao, Hongli
collection PubMed
description BACKGROUND: Transcription factor AP-2 alpha (TFAP2A) has been reported to participate in various tumors. However, the transcriptional levels and prognostic values of TFAP2A remain elusive in lung adenocarcinoma (LUAD). The purpose of the present study was to investigate the impact of the TFAP2A in LUAD. METHODS: The transcriptional levels and prognostic effects of TFAP2A were explored in patients with LUAD using various online databases, including the GEPIA, Oncomine, and Kaplan-Meier plotter databases. Meanwhile, meta-analyses were performed to verify the expression levels and prognostic effects of TFAP2A in LUAD using the Lung Cancer Explorer (LCE) database. In addition, target genes of TFAP2A were identified in the Animal TFDB3.0 dataset. RESULTS: Our comprehensively study indicated the mRNA expression levels of TFAP2A in LUAD were significantly higher than that of normal controls. In the survival analyses, higher TFAP2A levels were related to the shortened survival time of patients with LUAD. Meanwhile, the meta-analyses based on the LCE database also suggested the overexpressed TFAP2A led to worsen prognosis of patients with LUAD. Finally, the cell division cycle 6 (CDC6) and aurora kinase A (AURKA) were regarded as two target genes of TFAP2A. CONCLUSIONS: We have performed comprehensive analyses for TFAP2A in patients with LUAD. Patients with higher TFAP2A levels demonstrated worsen prognosis than those with lower TFAP2A levels. The CDC6 and AURKA might be two target genes of TFAP2A. Further molecular biological experiments were required to study the mechanisms of TFAP2A in LUAD.
format Online
Article
Text
id pubmed-8799082
institution National Center for Biotechnology Information
language English
publishDate 2020
publisher AME Publishing Company
record_format MEDLINE/PubMed
spelling pubmed-87990822022-02-02 The comprehensive investigation of transcription factor AP-2 alpha in lung adenocarcinoma Liao, Hongli Lin, Peng Transl Cancer Res Original Article BACKGROUND: Transcription factor AP-2 alpha (TFAP2A) has been reported to participate in various tumors. However, the transcriptional levels and prognostic values of TFAP2A remain elusive in lung adenocarcinoma (LUAD). The purpose of the present study was to investigate the impact of the TFAP2A in LUAD. METHODS: The transcriptional levels and prognostic effects of TFAP2A were explored in patients with LUAD using various online databases, including the GEPIA, Oncomine, and Kaplan-Meier plotter databases. Meanwhile, meta-analyses were performed to verify the expression levels and prognostic effects of TFAP2A in LUAD using the Lung Cancer Explorer (LCE) database. In addition, target genes of TFAP2A were identified in the Animal TFDB3.0 dataset. RESULTS: Our comprehensively study indicated the mRNA expression levels of TFAP2A in LUAD were significantly higher than that of normal controls. In the survival analyses, higher TFAP2A levels were related to the shortened survival time of patients with LUAD. Meanwhile, the meta-analyses based on the LCE database also suggested the overexpressed TFAP2A led to worsen prognosis of patients with LUAD. Finally, the cell division cycle 6 (CDC6) and aurora kinase A (AURKA) were regarded as two target genes of TFAP2A. CONCLUSIONS: We have performed comprehensive analyses for TFAP2A in patients with LUAD. Patients with higher TFAP2A levels demonstrated worsen prognosis than those with lower TFAP2A levels. The CDC6 and AURKA might be two target genes of TFAP2A. Further molecular biological experiments were required to study the mechanisms of TFAP2A in LUAD. AME Publishing Company 2020-03 /pmc/articles/PMC8799082/ /pubmed/35117502 http://dx.doi.org/10.21037/tcr.2020.01.58 Text en 2020 Translational Cancer Research. All rights reserved. https://creativecommons.org/licenses/by-nc-nd/4.0/Open Access Statement: This is an Open Access article distributed in accordance with the Creative Commons Attribution-NonCommercial-NoDerivs 4.0 International License (CC BY-NC-ND 4.0), which permits the non-commercial replication and distribution of the article with the strict proviso that no changes or edits are made and the original work is properly cited (including links to both the formal publication through the relevant DOI and the license). See: https://creativecommons.org/licenses/by-nc-nd/4.0/.
spellingShingle Original Article
Liao, Hongli
Lin, Peng
The comprehensive investigation of transcription factor AP-2 alpha in lung adenocarcinoma
title The comprehensive investigation of transcription factor AP-2 alpha in lung adenocarcinoma
title_full The comprehensive investigation of transcription factor AP-2 alpha in lung adenocarcinoma
title_fullStr The comprehensive investigation of transcription factor AP-2 alpha in lung adenocarcinoma
title_full_unstemmed The comprehensive investigation of transcription factor AP-2 alpha in lung adenocarcinoma
title_short The comprehensive investigation of transcription factor AP-2 alpha in lung adenocarcinoma
title_sort comprehensive investigation of transcription factor ap-2 alpha in lung adenocarcinoma
topic Original Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8799082/
https://www.ncbi.nlm.nih.gov/pubmed/35117502
http://dx.doi.org/10.21037/tcr.2020.01.58
work_keys_str_mv AT liaohongli thecomprehensiveinvestigationoftranscriptionfactorap2alphainlungadenocarcinoma
AT linpeng thecomprehensiveinvestigationoftranscriptionfactorap2alphainlungadenocarcinoma
AT liaohongli comprehensiveinvestigationoftranscriptionfactorap2alphainlungadenocarcinoma
AT linpeng comprehensiveinvestigationoftranscriptionfactorap2alphainlungadenocarcinoma