Gastric cancer (GC), one of the most prevalent malignancies across the world, has an increasing incidence rate. Long non-coding RNA (lncRNA) PURPL (also referred to as LINC01021) has been demonstrated to influence malignant GC behaviors and partake in other cancers. Notwithstanding, reports pertaining to the underlying mechanism of PURPL in GC haven't been rarely seen. Presently, in-vivo and ex-vivo experiments were implemented to examine the PURPL-miR-137-ZBTB7A-PI3K-AKT-NF-κB regulatory axis in GC. Our statistics revealed that PURPL presented a high expression in GC tissues and cell lines. PURPL overexpression remarkably exacerbated colony formation, migration, and invasion and repressed apoptosis in GC cells (AGS and MNK-45). In-vivo experiments also corroborated that cell growth was boosted by PURPL up-regulation. Mechanistic investigations verified that PURPL interacted with miR-137 and lowered its profile in GC cell lines. miR-137 overexpression or ZBTB7A knockdown upended the oncogenic function mediated by PURPL. PURPL initiated the PI3K/AKT/NF-κB pathway. PI3K and NF-κB inhibition impaired the promoting impact on GC cells elicited by PURPL overexpression and contributed to PURPL down-regulation. These findings disclosed that PURPL serves as an oncogene in the context of GC via miR-137-ZBTB7A-PI3K-AKT-NF-κB axis modulation.
Keywords: Gastric cancer; PURPL; ZBTB7A; miR-137; progression; signaling pathway.