Investigation of hnRNPK's role in gastric cancer proliferation and migration and its interaction with TL1A.

The present investigation elucidated the pivotal involvement of heterogeneous nuclear ribonucleoprotein K (hnRNPK) in the oncogenic advancement of gastric carcinoma through an integrative, multi-tiered analytical framework. Quantitative tissue microarray assessments indicated that elevated hnRNPK abundance exhibited a marked association with tumor differentiation grade, lymphatic dissemination, TNM classification, and unfavorable clinical outcome. Mechanistic exploration further substantiated that hnRNPK, predominantly confined to the nuclear compartment, facilitates gastric tumor aggressiveness by modulating the PI3K/Akt transduction cascade. Both in vivo and in vitro assays consistently verified that hnRNPK markedly augments the proliferative and motile potentials of gastric carcinoma cells. Importantly, this research constitutes the initial report delineating a molecular linkage between hnRNPK activity and gastric cancer pathogenesis. Rescue experiments demonstrated that TL1A knockdown in hnRNPK-overexpressing cells significantly reversed pro-tumor phenotypes, suggesting that hnRNPK exerts its oncogenic effects at least partially through a TL1A-dependent mechanism. These findings not only provide insights into the molecular mechanism of hnRNPK in GC but also offer experimental evidence for developing novel therapeutic strategies targeting the hnRNPK-TL1A axis in GC.