MicroRNA-663 antagonizes apoptosis antagonizing transcription factor to induce apoptosis in epithelial cells.
Apoptosis
/ drug effects
Apoptosis Regulatory Proteins
/ antagonists & inhibitors
Cells, Cultured
Down-Regulation
/ drug effects
Epithelial Cells
/ drug effects
Gingiva
/ cytology
HEK293 Cells
Humans
MCF-7 Cells
MicroRNAs
/ pharmacology
Repressor Proteins
/ antagonists & inhibitors
Transcription Factors
/ antagonists & inhibitors
ApoptomiRs
Cell death
MicroRNAs
Porphyromonas gingivalis
Primary oral epithelial cells
Journal
Apoptosis : an international journal on programmed cell death
ISSN: 1573-675X
Titre abrégé: Apoptosis
Pays: Netherlands
ID NLM: 9712129
Informations de publication
Date de publication:
02 2019
02 2019
Historique:
pubmed:
6
1
2019
medline:
21
4
2020
entrez:
6
1
2019
Statut:
ppublish
Résumé
MicroRNAs are small functional RNAs that modulate various biological processes in cells by interfering with gene translation. We have previously demonstrated that certain miRNAs play a crucial role in the innate immune responses of human oral epithelial cells to Porphyromonas gingivalis. While addressing the mechanisms of P. gingivalis induced apoptosis in these cells, we discovered that certain miRNAs are upregulated upon stimulation with live bacteria. These upregulated miRNAs include hsa-miR-584, hsa-miR-572, hsa-miR-210, hsa-miR-492, hsa-miR-623 and hsa-miR-663. Further analysis revealed an unexpected role for hsa-miR-663 (miR-663). To further evaluate miR-663 function, we overexpressed miR-663 in epithelial cells which resulted in cellular apoptosis. The bioinformatics analysis of the miR-663 target prediction, revealed a strong binding affinity to a 3' UTR region of Apoptosis Antagonizing Transcription Factor (AATF) mRNA. To demonstrate the binding of miR-663 to AATF mRNA, the putative miR-663 target site within the 3'-UTR region of AATF was cloned in luciferase vector and transfected to HEK293T cells. Luminescence data showed the downregulation of luciferase activity in cells that had the full length target region of the putative binding site, confirming that AATF is one of the targets for miR-663. This prompted us to further evaluate its role in a cancer cell line (MCF-7) to determine miR-663s' apoptotic function. The overexpression of miR-663 led to a significant increase in apoptosis of MCF-7 cells. Taken together, miR-663 may function as an 'apoptomiR' by inhibiting the anti-apoptotic gene AATF to induce apoptosis. These findings could have therapeutic implications for epithelial cell targeting in cancer therapy.
Identifiants
pubmed: 30610504
doi: 10.1007/s10495-018-01513-9
pii: 10.1007/s10495-018-01513-9
doi:
Substances chimiques
AATF protein, human
0
Apoptosis Regulatory Proteins
0
MIRN663 microRNA, human
0
MicroRNAs
0
Repressor Proteins
0
Transcription Factors
0
Types de publication
Journal Article
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
108-118Subventions
Organisme : NIDCR NIH HHS
ID : R01 DE024160
Pays : United States
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