https://www.selleckchem.com/products/Teniposide(Vumon).html LncRNA RAMS11 promoted cell growth and metastasis of prostate cancer cells. Down-regulation of lncRNA RAMS11 attenuated cell growth and metastasis of prostate cancer cells. We also demonstrated that lncRNA RAMS11 bound to CBX4 to activate expression of Top2α. LncRNA RAMS11 promoted tumor growth of prostate cancer in the mouse model. The inhibition of CBX4 attenuated the pro-cancer effects of lncRNA AMS11 in prostate cancer cells, while the activation of Top2α attenuated the anti-cancer effects of si-lncRNA RAMS11 in prostate cancer cells. Our results indicated that lncRNA RAMS11 promoted cell growth and metastasis of prostate cancer by CBX4 complex via binding to Top2α, and might be developed for the treatment of prostate cancer. Our results indicated that lncRNA RAMS11 promoted cell growth and metastasis of prostate cancer by CBX4 complex via binding to Top2α, and might be developed for the treatment of prostate cancer. Linc-ROR is a long non-coding RNA, that is found aberrantly expressed in various human cancers. We aim here to unveil the role of Linc-ROR in gastric cancer (GC) progression. qPCR was used to determine gene expression. Cell viability was measured by CCK-8 assay. Transwell assays were performed to evaluate the GC cells' migratory and invasive abilities. Xenograft mouse model was conducted to measure tumor growth. We found that Linc-ROR were overexpressed in GC tissues compared to the adjacent tissues. High Linc-ROR predicts poor prognosis of GC patients. The prediction of bioinformatics online revealed that Linc-ROR could bind to miR-212-3p. Further, dual-luciferase reporter assay confirmed a direct interaction between Linc-ROR and miR-212-3p. Overexpression of miR-212-3p facilitated GC cells' migration and invasion, while the silencing of miR-212-3p attenuated GC cell migratory and invasive abilities. Moreover, Linc-ROR knockdown significantly suppressed the proliferation, migration, and in