Long non-coding RNA (FALEC), as a lncRNA, Promotes Malignant Behaviors of Gastric Cancer Cells by Regulating miR-203b/PIM3 Axis
Abstract BackgroundPieces of evidences have shown the important regulatory effects of long non-coding RNAs (lncRNAs) in gastric cancer (GC). While it is not entirely clear for the role and mechanism of focally amplified lncRNA on chromosome 1 (FALEC) during GC tumorigenesis. MethodsThe levels of FALEC, microRNA-203b (miR-203b), and PIM3 were confirmed by qRT-PCR. And cell autophagy, proliferation, apoptosis, migration, and invasion were estimated using western blot for autophagy-related proteins, Transmission electron microscopy (TEM), CCK-8, flow cytometer, and Transwell assays in NCI-N87 cells and Xenograft tumor. Besides, the interaction between miR-203b and FALEC or PIM3 was verified using a dual-luciferase reporter assay. Moreover, the involvement of miR-203b and PIM3 in the regulatory effects of FALEC on GC was determined by rescue experiments. ResultsThe results proved that FALEC and PIM3 were highly expressed, while miR-203b was lowly expressed in GC. FALEC knockdown repressed GC cell proliferation, migration, and invasion, promoted apoptosis and autophagy in vitro. Meanwhile, FALEC knockdown prevented growth and induced GC autophagy in vivo. In mechanism, FALEC could upregulate PIM3 by sponging miR-203b in GC cells. Besides, FALEC induced the malignant behaviors of GC cells by regulating the miR-203b/PIM3 axis. ConclusionsTherefore, FALEC/miR-203b/PIM3 axis might act as the promising therapeutic target for the therapy of GC patients.