Background: Colorectal cancer (CRC), a malignant tumor, has become a highly relevant social problem. Nuclear paraspeckle assembly transcript 1 (NEAT1) was reported as an oncogenic long noncoding RNA in diverse tumors, including CRC. Nevertheless, the mechanism of NEAT1 in CRC remains unknown. Materials and Methods: The expression levels of NEAT1 and solute carrier family 38 member 1 (SLC38A1) 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 SLC38A1 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 NEAT1 or SLC38A1 was predicted by StarBase or TargetScan, and verified by the dual-luciferase reporter assay. The effect of NEAT1 on tumor growth was determined in CRC mice model. Results: The expression of NEAT1 and SLC38A1 was upregulated in CRC tissues and cells. NEAT1 knockdown or SLC38A1 downregulation restrained cell proliferation and invasion, and accelerated cell apoptosis and autophagy of CRC cells. NEAT1 acted as a sponge of miR-138 to regulate SLC38A1 expression. Furthermore, NEAT1 deficiency suppressed tumor growth in vivo. Conclusion: These studies disclosed that NEAT1 knockdown inhibited CRC progression by miR-138/SLC38A1 axis, providing an underlying target for CRC treatment.
Keywords: NEAT1; SLC38A1; colorectal cancer; miR-138.