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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 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 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). 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.

PurposeThis study aims to evaluate the effect of dimercaptosuccinic acid (DMSA)-coated superparamagnetic iron oxide (γ-Fe2O3@DMSA) bearing the 2-deoxy-d-glucose (2-DG) ligand on targeting tumors with high-glucose metabolism.Proceduresγ-Fe2O3@DMSA and 2-DG-conjugated γ-Fe2O3@DMSA (γ-Fe2O3@DMSA-DG) were prepared. The glucose consumption of MDA-MB-231 and MCF-7 breast cancer cells and human mammary epithelial cells (HMEpiCs) was assessed. Cells were incubated with γ-Fe2O3@DMSA or γ-Fe2O3@DMSA-DG, and MDA-MB-231 cells which exhibited the highest glucose consumption were used in breast cancer xenografts. Tumor targeting was studied by magnetic resonance imaging and Prussian blue staining in vivo.ResultsGlucose consumption was highest in MDA-MB-231 and lowest in HMEpiCs. In vitro, there was significant uptake of γ-Fe2O3@DMSA-DG by MDA-MB-231 and MCF-7 cells within 2 h and this was inhibited by glucose. Uptake of γ-Fe2O3@DMSA-DG was significantly higher in MDA-MB-231 compared with MCF-7 cells, and there was no obvious uptake of γ-Fe2O3@DMSA in either cell line. In vivo, γ-Fe2O3@DMSA-DG could be detected in the liver and in tumors post-injection, while γ-Fe2O3@DMSA was nearly undetectable in tumors.Conclusions2-DG-coated γ-Fe2O3@DMSA improved tumor targeting of γ-Fe2O3@DMSA which can be assessed by magnetic resonance imaging.