Aurora Kinase A: The Prominent Oncogenic Link in Helicobacter pylori-Driven Gastric Carcinogenesis

Abstract

Chronic Helicobacter pylori (H. pylori) infection leads to gastric carcinoma (GC), while aurora kinase A (AURKA) is known to be upregulated in several cancers. However, the direct association between AURKA and H. pylori remains largely unexplored. The significance of AURKA in H. pylori infection was investigated using an RNAi-mediated silencing method. The expression of downstream signaling genes and apoptotic markers was analyzed through qRT-PCR and western blot. Cancerous properties were evaluated through scratch wound assay, cell counting through trypan blue, and genomic instability assay. We used RNAi-mediated gene silencing to knock down AURKA expression and observed a reduction in the transcript levels of H. pylori pathogenic genes, signaling genes associated with H. pylori infection. We found that AURKA regulated STAT3 and c-Myc, which further enhanced the oncogenic potential of H. pylori. Moreover, AURKA knockdown led to the activation of apoptotic markers and alterations in mitochondrial biomass and membrane potential during H. pylori infection. Additionally, AURKA knockdown reduced cell proliferation, migration, and genomic instability in H. pylori-infected AGS cells. This study demonstrates that AURKA knockdown could abrogate H. pylori-induced expression of STAT3 and c-Myc in AGS, suggesting a functional signaling axis linking AURKA to H. pylori-mediated downstream effects.