Gastric cancer is the third leading cause of
cancer-related deaths worldwide, and research on
gastric cancer pathogenesis is fundamental. Long intergenic non-coding RNAs (
lincRNAs) control
cancer initiation and progression through several mechanisms, with the
competitive endogenous RNA (
ceRNA) regulatory network being the most common. In this study, in situ hybridization revealed that
long intergenic non-protein coding RNA-regulator of reprogramming (linc-ROR) was highly expressed in
gastric cancer cells and was mainly cytoplasmic-positive. Cell counting kit-8 (CCK-8), plate colony formation, wound healing, and Transwell assay revealed that linc-ROR knockdown impedes the growth, proliferation, and migration of
gastric cancer cells, while linc-ROR overexpression promoted
gastric cancer cell growth, migration, and colony formation ability. Combined with previous studies, the molecular mechanism axis of linc-ROR/miR-145-5-5p/POU5F1/SOX2 was verified. The expression of linc-ROR knockdown significantly suppressed the
protein expression of POU5F1 and SOX2. Co-transfection with linc-ROR
siRNA reverses the carcinogenic effect of the miR-145-5p inhibitor on
gastric cancer cell proliferation, cloning, and migration. These findings lay a foundation for developing novel targets for
gastric cancer treatment.