MicroRNA-142-3p promotes renal cell carcinoma progression by targeting RhoBTB3 to regulate HIF-1 signaling and GGT/GSH pathways.
Journal
Scientific reports
ISSN: 2045-2322
Titre abrégé: Sci Rep
Pays: England
ID NLM: 101563288
Informations de publication
Date de publication:
12 04 2023
12 04 2023
Historique:
received:
03
02
2022
accepted:
27
09
2022
medline:
14
4
2023
entrez:
12
4
2023
pubmed:
13
4
2023
Statut:
epublish
Résumé
MicroRNAs play a critical regulatory role in different cancers, but their functions in renal cell carcinoma (RCC) have not been elucidated. Reportedly, miR-142-3p is involved in the tumorigenesis and the development of RCC in vitro and is clinically correlated with the poor prognosis of RCC patients. However, the molecular target of miR-142-3p and the underlying mechanism are unclear. In this study, we found that miR-142-3p was upregulated in RCC tumor tissues and downregulated in exosomes compared to normal tissues. The expression of miR-142-3p was inversely associated with the survival of patients with kidney renal clear cell carcinoma (KIRC). RhoBTB3 was reduced in RCC, and miR-142-3p plays an inverse function with RhoBTB3 in KIRC. The direct interaction between RhoBTB3 and miR-142-3p was demonstrated by a dual luciferase reporter assay. miR-142-3p promoted metastasis in the xenograft model, and the suppression of miR-142-3p upregulated RhoBTB3 protein expression and inhibited the mRNAs and proteins of HIF1A, VEGFA, and GGT1. Also, the miR-142-3p overexpression upregulated the mRNA of HIF1A, VEGFA, and GGT1. In conclusion, miR-142-3p functions as an oncogene in RCC, especially in KIRC, by targeting RhoBTB3 to regulate HIF-1 signaling and GGT/GSH pathways, which needs further exploration.
Identifiants
pubmed: 37045834
doi: 10.1038/s41598-022-21447-2
pii: 10.1038/s41598-022-21447-2
pmc: PMC10097650
doi:
Substances chimiques
MicroRNAs
0
RhoBTB3 protein, human
EC 3.6.5.2
rho GTP-Binding Proteins
EC 3.6.5.2
MIRN142 microRNA, human
0
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
5935Informations de copyright
© 2023. The Author(s).
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