EphB4 knockdown inhibits the growth and epithelial–mesenchymal transition of gastric cancer cells and triggers death via the PI3K/AKT pathway.

Introduction:

The management of gastric cancer is challenging due to the complexities associated with its therapy and nursing care. This work aimed to elucidate the functions and processes of erythropoietin-producing hepatocellular carcinoma Receptor B4 (EphB4) in gastric cancer.

Methods:

EphB4 expression in gastric cancer tissues and cell lines was assessed using RT-qPCR and Western blotting techniques. The impact of EphB4 on cell growth, programmed cell death, transformation of cells from an epithelial to a mesenchymal state, and the PI3K/AKT signaling pathway in gastric cancer cells was also examined by MTT tests, flow cytometry, and Western blotting.

Results:

EphB4 expression was significantly increased (P<0.05) in gastric cancer tissues and cells. At the same time, downregulation of EphB4 significantly suppressed (P<0.001) gastric cancer cell proliferation, triggered apoptosis, reduced the expression of proteins associated with epithelial–mesenchymal transition (EMT), and exerted a regulatory influence by inhibiting the PI3K/AKT signaling pathway. Furthermore, the results revealed that the over-expression of EphB4 had a substantial impact on the proliferation of (P<0.001) gastric cancer cells, suppressing apoptosis, reducing the expression of E-cadherin, increasing the expression of N-cadherin, and activating the PI3K/AKT signaling pathway. The suppression of EphB4 significantly impeded (P<0.001) the cell growth and epithelial–mesenchymal transition (EMT) process while promoting apoptosis in gastric cancer cells.

Conclusion:

These discoveries provide new perspectives on the involvement of EphB4 in the progression of gastric cancer. All this makes EphB4 a promising target for future study in gastric cancer.