LncRNA SLC7A11-AS1 Contributes to Lung Cancer Progression Through Facilitating TRAIP Expression by Inhibiting miR-4775.
Onco Targets Ther
; 13: 6295-6302, 2020.
Article
en En
| MEDLINE
| ID: mdl-32636648
ABSTRACT
PURPOSE:
Long non-coding RNAs (lncRNAs) are important regulators of lung cancer. This article introduced a novel lncRNA, SLC7A11-AS1, whose effects on lung cancer development have been explored.METHODS:
Lung cancer tissues and normal tissues of 47 patients were collected. Bronchial epithelial cell line (BEAS-2B) and lung cancer cell lines (H520, H596, A549 and H1299) were cultured. H1299 and A549 cells were transfected with siSLC7A11-AS1 or siNC. The proliferation, migration and invasion of H1299 and A549 cells were detected by CCK-8 assay and Transwell experiment. Caspase-3 activity in H1299 and A549 cells was researched using caspase-3 activity detection kit. Dual-luciferase reporter gene assay and RNA pull-down assay were performed to explore the relationship between SLC7A11-AS1 and miR-4775. SLC7A11-AS1, miR-4775 and TRAIP mRNA expressions in tissues/cells were detected by qRT-PCR.RESULTS:
The up-regulated SLC7A11-AS1 in lung cancer patients was associated with metastasis and advanced tumor stage (P < 0.05). SLC7A11-AS1 was significantly up-regulated in lung cancer cells (P < 0.05). Silencing of SLC7A11-AS1 prominently inhibited H1299 and A549 cells proliferation, migration and invasion in vitro (P < 0.05). SLC7A11-AS1 acted as a sponge to inhibit miR-4775 expression in H1299 and A549 cells. Meanwhile, TRAIP expression in H1299 and A549 cells was directly and negatively regulated by miR-4775. Inhibition of miR-4775 or overexpression of TRAIP in H1299 and A549 cells remarkably reversed the reduced proliferation, migration and invasion induced by SLC7A11-AS1 silencing (P < 0.05).CONCLUSION:
SLC7A11-AS1 promoted lung cancer development by enhancing TRAIP expression via suppressing miR-4775.
Texto completo:
1
Colección:
01-internacional
Base de datos:
MEDLINE
Idioma:
En
Revista:
Onco Targets Ther
Año:
2020
Tipo del documento:
Article