GBX2, as a tumor promoter in lung adenocarcinoma, enhances cells viability, invasion and migration by regulating the AKT/ERK signaling pathway.
A549 Cells
Adenocarcinoma of Lung
/ genetics
Cell Line, Tumor
Cell Movement
Cell Proliferation
Cell Survival
Extracellular Signal-Regulated MAP Kinases
/ metabolism
Female
Gene Expression Regulation, Neoplastic
Gene Knockdown Techniques
Homeodomain Proteins
/ genetics
Humans
Lung Neoplasms
/ genetics
MAP Kinase Signaling System
Male
Middle Aged
Neoplasm Invasiveness
Prognosis
Proto-Oncogene Proteins c-akt
/ metabolism
Up-Regulation
AKT/ERK signaling pathway
GBX2
invasion and migration
lung adenocarcinoma
proliferation
Journal
The journal of gene medicine
ISSN: 1521-2254
Titre abrégé: J Gene Med
Pays: England
ID NLM: 9815764
Informations de publication
Date de publication:
02 2020
02 2020
Historique:
received:
10
09
2019
revised:
07
11
2019
accepted:
20
11
2019
pubmed:
24
11
2019
medline:
15
5
2021
entrez:
24
11
2019
Statut:
ppublish
Résumé
Increasing evidence shows that gastrulation brain homeobox 2 (GBX2) is involved in multiple cancers. However, whether GBX2 has an effect on the lung adenocarcinoma remains unclear. In the present study, we investigated the functions of GBX2 on lung adenocarcinoma and explored the underlying mechanism. Public data were obtained from the TCGA (https://cancergenome.nih.gov) and Oncomine (http://www.oncomine.org) databases. GBX2 expression and its prognostic value were analyzed by bioinformatics methods. Relative mRNA and protein expression levels of GBX2 in lung adenocarcinoma cell lines were evaluated via a quantitative reverse transcriptase polymerase chain reaction and western blotting. Lung adenocarcinoma cell lines LTEP-a-2 and A549, respectively, were selected for gain and loss function of GBX2 assays. Cell viability was detected by CCK8 and clone formation experiments. Cell invasion and migration were assessed by Transwell assays. The effect of GBX2 on the AKT/extracellular signal regulated kinase (ERK) pathway was tested by western blotting. Compared to adjacent tissues, GBX2 expression was up-regulated in lung adenocarcinoma tissues. High expression of GBX2 led to a poor survival and could be seen as an independent predictor for lung adenocarcinoma patients. Furthermore, down-regulation of GBX2 notably restrained the viability, invasion and migration abilities of A549 cells, whereas up-regulation of GBX2 in LTEP-a-2 cells presented the opposite outcomes. Furthermore, western blot indicated that down-regulation of GBX2 decreases the protein levels of phosphorylated (p)-AKT and p-ERK in A549 cells, whereas up-regulation of GBX2 shows the opposite effects in LTEP-a-2 cells. The results of present study indicate that GBX2 acts a cancer-promoting role to accelerate cell proliferation, invasion and migration partly by modulation of the AKT/ERK pathway in lung adenocarcinoma.
Sections du résumé
BACKGROUND
Increasing evidence shows that gastrulation brain homeobox 2 (GBX2) is involved in multiple cancers. However, whether GBX2 has an effect on the lung adenocarcinoma remains unclear. In the present study, we investigated the functions of GBX2 on lung adenocarcinoma and explored the underlying mechanism.
METHODS
Public data were obtained from the TCGA (https://cancergenome.nih.gov) and Oncomine (http://www.oncomine.org) databases. GBX2 expression and its prognostic value were analyzed by bioinformatics methods. Relative mRNA and protein expression levels of GBX2 in lung adenocarcinoma cell lines were evaluated via a quantitative reverse transcriptase polymerase chain reaction and western blotting. Lung adenocarcinoma cell lines LTEP-a-2 and A549, respectively, were selected for gain and loss function of GBX2 assays. Cell viability was detected by CCK8 and clone formation experiments. Cell invasion and migration were assessed by Transwell assays. The effect of GBX2 on the AKT/extracellular signal regulated kinase (ERK) pathway was tested by western blotting.
RESULTS
Compared to adjacent tissues, GBX2 expression was up-regulated in lung adenocarcinoma tissues. High expression of GBX2 led to a poor survival and could be seen as an independent predictor for lung adenocarcinoma patients. Furthermore, down-regulation of GBX2 notably restrained the viability, invasion and migration abilities of A549 cells, whereas up-regulation of GBX2 in LTEP-a-2 cells presented the opposite outcomes. Furthermore, western blot indicated that down-regulation of GBX2 decreases the protein levels of phosphorylated (p)-AKT and p-ERK in A549 cells, whereas up-regulation of GBX2 shows the opposite effects in LTEP-a-2 cells.
CONCLUSIONS
The results of present study indicate that GBX2 acts a cancer-promoting role to accelerate cell proliferation, invasion and migration partly by modulation of the AKT/ERK pathway in lung adenocarcinoma.
Substances chimiques
GBX2 protein, human
0
Homeodomain Proteins
0
Proto-Oncogene Proteins c-akt
EC 2.7.11.1
Extracellular Signal-Regulated MAP Kinases
EC 2.7.11.24
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
e3147Informations de copyright
© 2019 John Wiley & Sons, Ltd.
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