Long Noncoding RNA Contributes to the Tumorigenesis of Colorectal Cancer Through Regulating Expression by Sponging miR-138.

Colorectal cancer (CRC), a malignant tumor, has become a highly relevant social problem. Nuclear paraspeckle assembly transcript 1 () was reported as an oncogenic long noncoding RNA in diverse tumors, including CRC. Nevertheless, the mechanism of in CRC remains unknown. The expression levels of and solute carrier family 38 member 1 () in CRC tissues and cells were detected by real-time quantitative polymerase chain reaction. The protein levels of p62, microtubule-associated protein light (LC3-I), LC3-II, and were examined by Western blot assay. Cell proliferation, apoptosis, and invasion were measured by 3-(4, 5-dimethyl-2-thiazolyl)-2, 5-diphenyl-2-H-tetrazolium bromide (MTT), and flow cytometry and transwell assays, respectively. The interaction between miR-138 and or was predicted by StarBase or TargetScan, and verified by the dual-luciferase reporter assay. The effect of on tumor growth was determined in CRC mice model. The expression of and was upregulated in CRC tissues and cells. knockdown or downregulation restrained cell proliferation and invasion, and accelerated cell apoptosis and autophagy of CRC cells. acted as a sponge of miR-138 to regulate expression. Furthermore, deficiency suppressed tumor growth These studies disclosed that knockdown inhibited CRC progression by miR-138/ axis, providing an underlying target for CRC treatment.