Objective      To investigate the effect of overexpression of suppressor of AP-1 and regulated by IFN (SARI) on the proliferation of cervical cancer cells and explore the underlying molecular mechanism.       Methods      HeLa cells and CaSki cells were transformed with plasmids capable of expressing SARI. The expression of SARI was detected by real-time PCR and Western blotting. Meanwhile

the proliferation of the transformed cancer cells was assessed by CCK-8 assay

and cell cycle and apoptosis were detected by flow cytometry. In addition

the transcriptional activity of AP-1 transcription factor was determined by luciferase reporter assay

and the expression of Mcl-1 and Bcl-2 was analyzed by Western blotting.       Results      A cell model of over-expressing SARI was successfully established (P0.01). After up-regulating SARI

the cell proliferation was inhibited

early apoptotic cells were increased

but no significant change was observed in the cell cycle. Moreover

the transcriptional activity of AP-1 and the expression of Mcl-1 were both significantly suppressed (P0.05)

while there was no change in the expression of Bcl-2.       Conclusion      Overexpression of SARI can induce early apoptosis of cervical cancer cells through suppressing the transcriptional activity of AP-1 and down-regulating the expression of Mcl-1.