STAT4-mediated down-regulation of miR-3619-5p facilitates stomach adenocarcinoma by modulating TBC1D10B.
Adaptor Proteins, Signal Transducing
/ genetics
Adenocarcinoma
/ genetics
Animals
Cell Line, Tumor
Disease Progression
Down-Regulation
Heterografts
Humans
Male
Mice
Mice, Inbred BALB C
Mice, Nude
MicroRNAs
/ genetics
STAT4 Transcription Factor
/ genetics
Signal Transduction
Stomach Neoplasms
/ genetics
Transfection
STAT4
TBC1D10B
miR-3619-5p
stomach adenocarcinoma
Journal
Cancer biology & therapy
ISSN: 1555-8576
Titre abrégé: Cancer Biol Ther
Pays: United States
ID NLM: 101137842
Informations de publication
Date de publication:
02 07 2020
02 07 2020
Historique:
pubmed:
14
5
2020
medline:
2
10
2021
entrez:
14
5
2020
Statut:
ppublish
Résumé
MicroRNAs (miRNAs) as the subtype of non-coding RNAs are revealed to be crucial players in cellular activities. It has been reported that miR-3619-5p functions as a tumor inhibitor in several cancers. However, the connection between miR-3619-5p and stomach adenocarcinoma (STAD) remains to be discovered. The purpose of the study is to figure out the role and molecular regulation mechanism of miR-3619-5p in STAD. The expression of miR-3619-5p was evaluated via qRT-PCR analysis. Gain-of-function experiments demonstrated the effects of miR-3619-5p on cellular functions. The upper-stream transcription factor STAT4 and downstream target gene TBC1D10B of miR-3619-5p were identified by bioinformatic analysis. The binding and interaction between the indicated molecules were verified by RNA pull-down and luciferase reporter assays. The expression of miR-3619-5p was prominently down-regulated in STAD cells and tissues. MiR-3619-5p suppresses cell proliferation, migration, invasion and tumor growth in STAD. Further, STAT4 bound with miR-3619-5p promoter and inhibited its transcription. MiR-3619-5p was also recognized to modulate STAD progression through the regulation of downstream target gene TBC1D10B. STAT4-mediated miR-3619-5p controls STAD carcinogenesis and progression through modulating TBC1D10B expression, which may provide a novel insight for researching the STAD-related molecular mechanism.
Sections du résumé
BACKGROUND
MicroRNAs (miRNAs) as the subtype of non-coding RNAs are revealed to be crucial players in cellular activities. It has been reported that miR-3619-5p functions as a tumor inhibitor in several cancers. However, the connection between miR-3619-5p and stomach adenocarcinoma (STAD) remains to be discovered.
AIM OF THE STUDY
The purpose of the study is to figure out the role and molecular regulation mechanism of miR-3619-5p in STAD.
METHODS
The expression of miR-3619-5p was evaluated via qRT-PCR analysis. Gain-of-function experiments demonstrated the effects of miR-3619-5p on cellular functions. The upper-stream transcription factor STAT4 and downstream target gene TBC1D10B of miR-3619-5p were identified by bioinformatic analysis. The binding and interaction between the indicated molecules were verified by RNA pull-down and luciferase reporter assays.
RESULTS
The expression of miR-3619-5p was prominently down-regulated in STAD cells and tissues. MiR-3619-5p suppresses cell proliferation, migration, invasion and tumor growth in STAD. Further, STAT4 bound with miR-3619-5p promoter and inhibited its transcription. MiR-3619-5p was also recognized to modulate STAD progression through the regulation of downstream target gene TBC1D10B.
CONCLUSION
STAT4-mediated miR-3619-5p controls STAD carcinogenesis and progression through modulating TBC1D10B expression, which may provide a novel insight for researching the STAD-related molecular mechanism.
Identifiants
pubmed: 32397798
doi: 10.1080/15384047.2020.1754690
pmc: PMC7515538
doi:
Substances chimiques
Adaptor Proteins, Signal Transducing
0
MIRN-3619 microRNA, human
0
MicroRNAs
0
STAT4 Transcription Factor
0
STAT4 protein, human
0
TBC1D10B protein, human
0
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
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