<b><i>Background:</i></b> The genomic copy number of LINC01061 is amplified in papillary thyroid cancer. However, its role in gastric cancer is not clear. <b><i>Materials and Methods:</i></b> Tissues and serum of GC patients were collected to detect the expression of LINC01061 by quantitative real-time polymerase chain reaction (qRT-PCR). ShRNA were applied to knock down the expression of LINC01061. Growth curves and colony formation experiments were applied to evaluate cell growth. Cell migration was assessed by transwell migration experiments. Cell cycle and apoptosis were analyzed by flow cytometry. Epithelial-mesenchymal transition (EMT) was examined by qRT-PCR and Western blot. <b><i>Results:</i></b> The expression of LINC01061 was upregulated in tissues and serum of GC patients and it was associated with the clinicopathological features and survival time. Functional study indicated that cell growth and migration were suppressed after LINC01061 knockdown. Cell cycle arrest and increased apoptosis occurred when LINC01061 expression was inhibited. EMT was also impaired combined with a decrease in β-catenin expression after LINC01061 knockdown. <b><i>Conclusions:</i></b> Our data indicate that LINC01061 is a novel biomarker for diagnosis and prognosis of GC. LINC01061 promoted progression of GC through cell cycle regulation and EMT.
MicroRNA-17 induces epithelial-mesenchymal transition consistent with the cancer stem cell phenotype by regulating CYP7B1 expression in colon cancer
