Lncrna SLC7A11-AS1 contributes to lung cancer progression through facilitating traip expression by inhibiting miR-4775

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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 pulldown assay were performed to explore the relationship between SLC7A11-AS1 and miR4775. 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 upregulated 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). SLC7A11AS1 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 miR4775. 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.

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Liu, Y., Fan, X., Zhao, Z., & Shan, X. (2020). Lncrna SLC7A11-AS1 contributes to lung cancer progression through facilitating traip expression by inhibiting miR-4775. OncoTargets and Therapy, 13, 6295–6302. https://doi.org/10.2147/OTT.S253082

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