Hsa_circ_0002019 promotes cell proliferation, migration, and invasion by regulating TNFAIP6/NF-?B signaling in gastric cancer

Background: Gastric cancer (GC) is a common cancer with a high incidence and mortality rate. Herein, the role of hsa_circ_0002019 (circ_0002019) in GC was investigated.Methods: The molecular structure and stability of circ_0002019 were identified by RNase R, and Actinomycin D treatment. Molecular associations were verified by RIP. Proliferation, migration, and invasion were detected by CCK-8, EdU, and Transwell, respectively. The effect of circ_0002019 on tumor growth was analyzed in vivo.Results: Circ_0002019 was elevated in GC tissues and cells. Circ_0002019 knockdown inhibited the proliferation, migration, and invasion. Mechanically, circ_0002019 activated NF-?B signaling by increasing TNFAIP6 mRNA stability by PTBP1. Activation of NF-?B signaling limited the antitumor effect of circ_0002019 silencing in GC. Circ_0002019 knockdown inhibited tumor growth in vivo by reducing TNFAIP6 expression.Conclusions: Circ_0002019 accelerated the proliferation, migration, and invasion by regulating TNFAIP6/NF-?B pathway, suggesting circ_0002019 could be a key regulatory factor in GC progression.

Automated summary

The role of circ_0002019 in gastric cancer (GC) was investigated in this study. It was found that circ_0002019 was highly expressed in GC tissues and cells. Silencing circ_0002019 suppressed the proliferation, migration, and invasion of GC cells. Mechanistically, circ_0002019 activated the NF-κB pathway by increasing the stability of TNFAIP6 mRNA through PTBP1. These findings indicate that circ_0002019 plays a critical regulatory role in the progression of GC.