Effects of forkhead Box protein A1 on cell proliferation regulating and EMT of cervical carcinoma.

Abstract

Cervical cancer is a common tumor in gynecological malignancies. However, the patients are often in an advanced stage when diagnosed. It was found that forkhead box protein A1 (FOXA1) is abnormally expressed in various tumors, such as breast cancer, ovarian cancer, and is closely related to tumorigenesis. This study aimed to investigate the expression and the related roles of FOXA1 in cervical cancer. Real Time-PCR (RT-PCR) and Western blot were used to analyze expression of FOXA1 in cervical cancer and adjacent tissue. The small-interfere RNA (siRNA) was adopted to down-regulate FOXA1 expression in HeLa cells. The effect of FOXA1 on apoptosis of HeLa cells was detected by using thiazolyl blue tetrazolium bromide (MTT) method. The apoptosis rate of HeLa cells was detected by using flow cytometry. The Western blot was selected to evaluate the epithelial mesenchymal transition (EMT) related protein, vimentin, E-cadherin, and vascular endothelial growth factor (VEGF) changes. Compared with adjacent tissues, FOXA1 mRNA and protein expressions significantly increased in cervical cancer (p<0.05). SiRNA significantly reduced FOXA1 expression in Hela cells compared with the control group and siRNA-NC group, thus inhibiting tumor cell proliferation and enhancing cell apoptosis rate (p<0.05). E-cadherin elevated, Vimentin decreased, and VEGF reduced after FOXA1 siRNA treatment. FOXA1 expression increased in cervical cancer. Inhibition of FOXA1 expression blocked the proliferation of cervical cancer, promoted tumor cell apoptosis, suppressed the occurrence of EMT and VEGF production, and can regulate cervical cancer metastasis. FOXA1 can be used as a new molecular biological target for cervical cancer diagnosis and treatment.