Knockdown of ephrin receptor A7 suppresses the proliferation and metastasis of A549 human lung cancer cells

Previous studies have demonstrated that ephrin (Eph) family receptor tyrosine kinases and ligands promote cancer growth, invasion and metastasis. In addition, it has been reported that Eph receptor A7 (EphA7) is transcriptionally activated in lung cancer; however, the effects of silencing EphA7 expression on the growth of lung cancer cells, and the underlying molecular mechanisms, have yet to be determined. Therefore, the present study aimed to investigate whether silencing EphA7 with small interfering (si) RNA could induce apoptosis in non-small cell lung cancer (NSCLC) cells. Furthermore, the effects of siEphA7 on cell migration and invasion were evaluated using Transwell assays. The mechanisms underlying the effects of siEphA7 on the tumorigenic properties of A549 cells were also examined. The results of the present study demonstrated that transfection with siEphA7 inhibited the proliferation, migration and invasion of A549 cells. In addition, siEphA7 significantly increased the protein expression levels of B-cell lymphoma 2 (Bcl-2)-associated X protein and caspase-3, and decreased the protein expression levels of Bcl-2, thus suggesting that siEphA7 was able to induce apoptosis via the intrinsic apoptotic pathway. In addition, the expression levels of phosphatase and tensin homolog (PTEN) were significantly upregulated, and the expression levels of total AKT were not altered, whereas the levels of phosphorylated-AKT were reduced. These findings indicated that EphA7 may have an important role in the pathogenesis of NSCLC by regulating PTEN expression via the PTEN/AKT pathway. Silencing EphA7 may provide a novel approach for the treatment of NSCLC.