DDX55 promotes hepatocellular carcinoma progression by interacting with BRD4 and participating in exosome-mediated cell-cell communication.
Carcinoma, Hepatocellular
/ pathology
Cell Communication
Cell Cycle Proteins
/ genetics
Cell Line, Tumor
Cell Proliferation
/ genetics
DEAD-box RNA Helicases
/ metabolism
Endothelial Cells
/ metabolism
Epithelial-Mesenchymal Transition
/ genetics
Exosomes
/ metabolism
Gene Expression Regulation, Neoplastic
Glycogen Synthase Kinase 3 beta
/ metabolism
Humans
Liver Neoplasms
/ pathology
Nuclear Proteins
/ genetics
Phosphatidylinositol 3-Kinases
/ metabolism
Transcription Factors
/ genetics
BRD4
DDX55
exosome
hepatocellular carcinoma
β-Catenin
Journal
Cancer science
ISSN: 1349-7006
Titre abrégé: Cancer Sci
Pays: England
ID NLM: 101168776
Informations de publication
Date de publication:
Sep 2022
Sep 2022
Historique:
revised:
26
04
2022
received:
09
02
2022
accepted:
30
04
2022
pubmed:
7
5
2022
medline:
14
9
2022
entrez:
6
5
2022
Statut:
ppublish
Résumé
The involvement of DEAD-box helicase 55 (DDX55) in oncogenesis has been suggested, but its biological role in hepatocellular carcinoma (HCC) remains unknown. The present study verified the upregulation of DDX55 in HCC tissues compared with non-tumor controls. DDX55 displayed the highest prognostic values among the DEAD-box protein family for recurrence-free survival and overall survival of HCC patients. In addition, the effects of DDX55 in the promotion of HCC cell proliferation, migration, and invasion were determined ex vivo and in vivo. Mechanistically, we revealed that DDX55 could interact with BRD4 to form a transcriptional regulatory complex that positively regulated PIK3CA transcription. Following that, β-catenin signaling was activated in a PI3K/Akt/GSK-3β dependent manner, thus inducing cell cycle progression and epithelial-mesenchymal transition. Intriguingly, both DDX55 mRNA and protein were identified in the exosomes derived from HCC cells. Exosomal DDX55 was implicated in intercellular communication between HCC cells with high or low DDX55 levels and between HCC cells and endothelial cells, thereby promoting the malignant phenotype of HCC cells and angiogenesis. In conclusion, DDX55 may be a valuable prognostic biomarker and therapeutic target in HCC.
Identifiants
pubmed: 35514200
doi: 10.1111/cas.15393
pmc: PMC9459289
doi:
Substances chimiques
BRD4 protein, human
0
Cell Cycle Proteins
0
Nuclear Proteins
0
Transcription Factors
0
Glycogen Synthase Kinase 3 beta
EC 2.7.11.1
DEAD-box RNA Helicases
EC 3.6.4.13
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
3002-3017Subventions
Organisme : Health Commission of Hubei Province Scientific Research Project
ID : WJ2021Z005
Organisme : Wuhan University
Informations de copyright
© 2022 The Authors. Cancer Science published by John Wiley & Sons Australia, Ltd on behalf of Japanese Cancer Association.
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