HNRNPAB is involved in the development of gastric cancer by regulating EMT through the AkT-GSK3β-Wnt signaling pathway

Background Gastric cancer (GC) is a leading cause of cancer-related death, and metastasis significantly contributes to poor prognosis. Splicing factors are known to influence cancer progression, including metastasis. This study aimed to investigate the role of heterogeneous nuclear ribonucleoprotein A/B (hnRNPAB) in GC cell invasion and migration. Methods An investigation into the role of hnRNPAB in GC was conducted. This study analyzed hnRNPAB expression in human gastric cancer tissues. Functional studies were then performed using gastric cancer cell lines with overexpression or knockdown of hnRNPAB to assess its effects on cell proliferation, migration, and invasion. Mechanistic studies were conducted to determine the signaling pathways involved in hnRNPAB-mediated effects. Results Overexpression of hnRNPAB in gastric cancer cell lines promoted cell proliferation, migration, and invasion. Conversely, hnRNPAB knockdown had the opposite effect. Mechanistically, hnRNPAB induced a switch in the expression of cell adhesion markers, increasing the expression of mesenchymal markers (N-cadherin, vimentin, and Snail1) while decreasing the expression of the epithelial marker E-cadherin, indicating its role in epithelial‒mesenchymal transition (EMT). Further investigation revealed that hnRNPAB activates the Akt-GSK3β-Wnt signaling pathway by promoting Akt phosphorylation and inactivating GSK3β. Conclusions These findings demonstrate that hnRNPAB promotes EMT and GC development by activating the Akt-GSK3β-Wnt signaling pathway. These findings suggest that hnRNPAB could be a potential target for developing novel diagnostic and therapeutic strategies for GC. Further studies are warranted to explore its therapeutic potential fully.