Investigation of the mechanism by which FOXJ2 inhibits proliferation, metastasis and cell cycle progression of ovarian cancer cells through the PI3K/AKT signaling pathway

Background As one member of the Forkhead Box transcription factor, Forkhead Box J2 (FOXJ2) is involved in diverse cancers. At present, the specific role and mechanism of FOXJ2 in ovarian cancer (OC) have not been fully addressed, which allows us to fill the blank. Materials and methods Accordingly, the expression of FOXJ2 in OC cells and ovarian epithelial cells was quantified via real-time qPCR. Following the transfection, cell counting kit-8, Transwell, wound healing and flow cytometry assays were performed to measure the proliferation, metastasis, apoptosis and cell cycle of OC cells A2780 and HEY. Further, real-time qPCR and Western blotting were both employed for the quantification assays on the expression levels of FOXJ2 as well as phosphoinositide 3-kinase (PI3K) and protein kinase B (AKT) (in both unphosphorylated and phosphorylated forms). Results Based on the results, FOXJ2 were highly-expressed in OC cells (P < 0.05). Silencing of FOXJ2 resulted in attenuated OC cell proliferation, reduced numbers of migrating and invading OC cells, decreased apoptotic capacity, and cell cycle arrest in G1/S phase (P < 0.05). In addition, the knockdown of FOXJ2 caused the downward trend on the phosphorylation level of both PI3K and AKT in OC cells (P < 0.05). Conclusion The silencing of FOXJ2 could repress the growth and metastasis potentials and cause the cell cycle G1/S arrest of OC cells in vitro, which was possibly achieved via targeting the PI3K/AKT pathway.