DDX10 promotes human lung carcinoma proliferation by U3 small nucleolar ribonucleoprotein IMP4.
DDX10
DEAD/H box RNA helicases
IMP4
U3 small nucleolar ribonucleoprotein
lung cancer
Journal
Thoracic cancer
ISSN: 1759-7714
Titre abrégé: Thorac Cancer
Pays: Singapore
ID NLM: 101531441
Informations de publication
Date de publication:
06 2021
06 2021
Historique:
revised:
10
04
2021
received:
30
01
2021
accepted:
12
04
2021
pubmed:
12
5
2021
medline:
5
1
2022
entrez:
11
5
2021
Statut:
ppublish
Résumé
Lung cancer is a common tumor and a leading cause of death worldwide. DEAD/H box RNA helicases (DDX) include several family members which regulate mRNA translation in cancer cells. In this study, we demonstrated that DEAD/H box RNA helicase 10 (DDX10) was significantly upregulated in lung cancer tissues compared with adjacent nontumor tissues. DDX10 expression was knocked down with shRNA in order to investigate the impact on A549 lung cancer cell growth and related molecular mechanisms in vitro and in vivo. DDX10 expression in lung cancer was assessed using online databases and patient samples. DDX10 knockdown significantly inhibited the proliferation of lung cancer cells in vitro and in vivo. Furthermore, the bioinformatic tool indicated the putative downstream protein U3 small nucleolar ribonucleoprotein 4 (IMP4). Our data showed a positive correlation between IMP4 and DDX10. We found that IMP4 overexpression could reverse the effect of DDX10 knockdown on the proliferation and apoptosis of A549 cells. The findings of this study suggest that DDX10/IMP4 might be a novel target for lung cancer diagnosis and treatment.
Sections du résumé
BACKGROUND
Lung cancer is a common tumor and a leading cause of death worldwide. DEAD/H box RNA helicases (DDX) include several family members which regulate mRNA translation in cancer cells. In this study, we demonstrated that DEAD/H box RNA helicase 10 (DDX10) was significantly upregulated in lung cancer tissues compared with adjacent nontumor tissues.
METHODS
DDX10 expression was knocked down with shRNA in order to investigate the impact on A549 lung cancer cell growth and related molecular mechanisms in vitro and in vivo. DDX10 expression in lung cancer was assessed using online databases and patient samples.
RESULTS
DDX10 knockdown significantly inhibited the proliferation of lung cancer cells in vitro and in vivo. Furthermore, the bioinformatic tool indicated the putative downstream protein U3 small nucleolar ribonucleoprotein 4 (IMP4). Our data showed a positive correlation between IMP4 and DDX10. We found that IMP4 overexpression could reverse the effect of DDX10 knockdown on the proliferation and apoptosis of A549 cells.
CONCLUSIONS
The findings of this study suggest that DDX10/IMP4 might be a novel target for lung cancer diagnosis and treatment.
Identifiants
pubmed: 33973712
doi: 10.1111/1759-7714.13976
pmc: PMC8201537
doi:
Substances chimiques
Ribonucleoproteins, Small Nucleolar
0
ribonucleoprotein, U3 small nucleolar
0
DDX10 protein, human
EC 3.6.1.-
DEAD-box RNA Helicases
EC 3.6.4.13
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
1873-1880Subventions
Organisme : Research Foundation of Beijing Friendship Hospital, Capital Medical University
ID : yyqdkt2018-27
Informations de copyright
© 2021 The Authors. Thoracic Cancer published by China Lung Oncology Group and John Wiley & Sons Australia, Ltd.
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