GATA6 inhibits the biological function of non-small cell lung cancer by modulating glucose metabolism.
GATA6
Glucose metabolism
Non-small cell lung cancer
c-Myc
Journal
Journal of cancer research and clinical oncology
ISSN: 1432-1335
Titre abrégé: J Cancer Res Clin Oncol
Pays: Germany
ID NLM: 7902060
Informations de publication
Date de publication:
14 Mar 2024
14 Mar 2024
Historique:
received:
28
01
2024
accepted:
23
02
2024
medline:
18
3
2024
pubmed:
14
3
2024
entrez:
14
3
2024
Statut:
epublish
Résumé
This study aims to explore the role of GATA6 in lung cancer, with a focus on its impact on metabolic processes. We assessed GATA6 expression in lung cancer tissues and its association with patient prognosis. In vitro cell function experiments were conducted to investigate the effects of altered GATA6 levels on lung cancer cell proliferation and migration. Mechanistic insights were gained by examining GATA6's influence on glucose metabolism-related genes, particularly its effect on c-Myc mRNA expression. Our study revealed significant down-regulation of GATA6 in lung cancer tissues, and this down-regulation was strongly correlated with unfavorable patient prognosis. Elevating GATA6 levels effectively inhibited the proliferation and migration of lung cancer cells in our cell function experiments. Mechanistically, we found that GATA6 suppressed the expression of c-Myc mRNA, impacting genes related to glucose metabolism. As a result, glucose uptake and metabolism in lung cancer cells were disrupted, ultimately impeding their malignant behaviors. Our study provides crucial insights into the metabolic regulation of GATA6 in lung cancer cells. These findings have the potential to offer a solid theoretical foundation for the development of novel clinical treatments for lung cancer.
Identifiants
pubmed: 38483616
doi: 10.1007/s00432-024-05664-y
pii: 10.1007/s00432-024-05664-y
pmc: PMC10940364
doi:
Substances chimiques
RNA, Messenger
0
Glucose
IY9XDZ35W2
GATA6 protein, human
0
GATA6 Transcription Factor
0
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
126Subventions
Organisme : Joint Fund Program Project of Liaodong University Research Fund
ID : 2022YB004
Organisme : Education Department in Liaoning Province
ID : LJKMZ20221762
Informations de copyright
© 2024. The Author(s).
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