ARHGAP17 suppresses tumor progression and up-regulates P21 and P27 expression via inhibiting PI3K/AKT signaling pathway in cervical cancer.

ARHGAP17 has long been thought to be involved in the maintenance of tight junction and epithelial barrier. Recently, a few Rho GTPase activating proteins (RhoGAPs) have been identified as tumor suppressors in some human cancers. The present study aimed to explore ARHGAP17 expression in cervical cancer and the possible function in tumor progression. ARHGAP17 expression in cervical cancer cell lines was assessed by RT-PCR and Western blotting. ARHGAP17 expression in cervical cancer tissues and normal tissues was assessed by immunohistochemistry. The cell proliferation was determined using CCK-8 in vitro and subcutaneous xenograft model in vivo. Here, we showed lower expression of ARHGAP17 in cell lines and human cervical cancer samples. Manipulation of ARHGAP17 affected cell proliferation in vitro and tumor growth in vivo. Furthermore, the phosphorylation of AKT was enhanced in ARHGAP17 silencing cervical cancer cells. ARHGAP17 can elevate P21 and P27 expression level through inhibiting PI3K/AKT signaling pathway. Stepwise investigations demonstrated that ARHGAP17 suppressed malignant phenotype of cervical cancer cells via inhibiting PI3K/AKT signaling pathway. These results reveal that ARHGAP17 functions as a tumor suppressor in cervical cancer that suppresses tumor growth, at least partly, through inhibition of PI3K/AKT signaling and up-regulation of P21 and P27 expression.