We then conducted a series of in vivo and in vitro assays to explore the effect of LINC01410 on miR-532-5p-mediated GC malignancy and the underlying mechanism involved. MiR-532-5p overexpression inhibited GC metastasis and angiogenesis in vitro and in vivo,whereas miR-532-5p silencing had the opposite effect. Further study showed that miR-532-5p attenuated NF-kB signaling by directly inhibiting NCF2 expression, while miR-532-5p silencing in GC enhanced NF-kB activity. Furthermore,we demonstrated miR-532-5p down-regulation was caused by aberrantly high expression of LINC01410 in GC. Mechanistically, overexpression of LINC01410 promoted GC angiogenesis and metastasis by binding to and suppressing miR-532-5p, which resulted in up-regulation of NCF2 and sustained NF-kB pathway activation.Interestingly, NCF2 could in turn increase the promoter activity and expression of LINC01410 via NF-kB, thus forming a positive feedback loop that drives the malignant behavior of GC. For instance, lncRNA HCP5 up-regulates expression of Runt-related transcription factor 1 (RUNX1) in glioma cells, while overexpression of RUNX1 can also up-regulate HCP expression.