Previously, we found that sperm-associated antigen 5 (SPAG5) was upregulated in 
pelvic lymph node metastasis-positive cervical cancer. The aim of this study is 
to examine the role of SPAG5 in the proliferation and tumorigenicity of cervical 
cancer and its clinical significance in tumor progression. In our study, SPAG5 
expression in cervical cancer patients was detected using quantitative real-time 
polymerase chain reaction, western blotting, and immunohistochemistry; cervical 
cancer cell function with downregulated SPAG5 in vitro was explored using 
tetrazolium assay, flow cytometry, and colony formation and Transwell assays. 
SPAG5 was upregulated in tumor tissue compared with paired adjacent noncancerous 
tissues; SPAG5 upregulation in tumor tissues indicated poor disease-free 
survival, which was also an independent prognostic indicator for cervical cancer 
patients. In vitro study demonstrated that SPAG5 downregulation inhibited cell 
proliferation and growth significantly by G2/M arrest and induction of 
apoptosis, and hindered cell migration and invasion. Under SPAG5 downregulation, 
the sensitivity of cervical cancer cells differed according to taxol dose, which 
correlated with mammalian target of rapamycin (mTOR) signaling pathway activity. 
In general, SPAG5 upregulation relates to poor prognosis in cervical cancer 
patients, and SPAG5 is a regulator of mTOR activity during taxol treatment in 
cervical cancer.