Helicobacter pylori induce circ_0046854 to regulate microRNA‐511‐3p/CSF1 axis and enhance the resistance of gastric cancer to cisplatin

Helicobacter pylori (HP) is considered a major risk factor for gastric cancer (GC) and during this process, cytotoxin‑associated gene A (CagA) plays in essence. The study mainly focused on the molecular mechanism of circular RNA 0046854 (circ_0046854) in HP‐induced GC. Clinically, 56 cases of GC and normal tissues were collected, and the GC tissues were divided into HP‐negative GC tissues (HP − ) and 33 HP‐positive GC tissues (HP + ). Tissue expression of circ_0046854, microRNA (miR)‐511‐3p and colony‐stimulating factor 1 (CSF1) was tested. BGC‐823/Cisplatin (DDP) resistant strain was induced and cell growth and DDP resistance were detected after HP infection. In vivo experiments were performed using a mouse xenograft model. The relationship between circ_0046854, miR‐511‐3p and CSF1 was confirmed. GC tissues especially HP + cancer tissues expressed high circ_0046854 and CSF1 and low miR‐511‐3p. HP‐induced circ_0046854 expression in GC cells through CagA. Inhibition of circ_0046854 or miR‐511‐3p elevation inhibited the growth and DDP resistance in GC cells. Circ_0046854 acted as a sponge for miR‐511‐3p, which targeted CSF1. Restoring CSF1 could abolish the inhibitory effect of miR‐511‐3p overexpression on CagA + HP‐induced GC progression in vitro. Circ_0046854 silencing repressed tumor growth and aggrandized the inhibiting effects of DDP on tumorigenesis in vivo . Circ_0046854/miR‐511‐3p/CSF1 axis may be involved in the development of HP‐induced GC, thus providing new ideas for studying the mechanism of HP‐related gastric diseases.