Aim Ovarian cancer has been one of most common cancers in women of all ages. Aspirin, previously known as an anti-inflammatory agent, was considered to be effective in ovarian cancer prevention and treatment. In this study, it aimed to comprehensively demonstrate the effects of aspirin on human ovarian cells HO8910 from many different stages of cell growth, differentiation and migration. Therefore, all relevant cell processes were ana- lyzed, including cell surface markers expression, cell viability, cell proliferation, cell migration, cell clustering; cell apoptosis and mitochondria membrane potential. The expression levels of relevant proteins were also provided. Finally, the potential mechanism for its inhibitory effects on cancer cells was demonstrated with cell apoptosis and cytokines regulation. Methods To explore the studies, the effects of aspirin on human ovarian cells HO8910 were comprehensively demonstrated, including cell characteristics involving cell surface markers expression CD44 ＋ and CD133 ＋, cell viability, cell proliferation, cell migration, cell clustering; cell apoptosis and mitochondria mem- brane potential; potential mechanism involving relevant proteins expression. The effects of Aspirin on human ovari- an cells were described from many different stages of cell growth, differentiation and migration. In addition, the po- tential mechanisms were demonstrated from cell apoptosis and proteins expression. Results The aspirin concentra- tions in treating cells HO8910 were range from 10, 5, 2 mmol · L^-1. VB2 was involved as controls with suggested concentration range from 40, 20, 10 mmol · L^-1. The cell surface markers percentages of CD44 ＋ and CD133 ＋ cells were decreased in both Aspirin and VB2 treated human ovarian cells （less than 80% ） , compared to that of control group （86%）. Cell proliferation viability, when the concentration of aspirin was 20 mmol · L^-1, the cell viability can be less than 40% of control and after 48 h and 72 h, the cell viability in Aspirin treated group contin- ued to be decreased, approaching 0%. For VB2, a concentration range wider than suggested concentration was in- volved in this detection （0. 25 - 100 μmol · L^-l）. After the first 24 h of VB2 treatment, the cell viability re- mained to be higher than 80 % of blank control. Colony formation of cells. The increased Aspirin concentration would lead to significantly decreased colony formation. Cell apoptosis, In aspirin treated groups, the ratio of cell ap- optosis （3%- 20% ） were greatly increased compared with control group （0.5%）, The expression of NK-KB and TNF-α,In Aspirin treated group, the expression level of TNF-α was increased with high concentration of aspirin, while the level of NK-KB was negative correlated with the level of TNF-α, which were down-regulated compared to control group. Conclusions In this study, the inhibitory effects of Aspirin on human ovarian cells HO8910 were demonstrated and analyzed. The cell viability, migration and colony formation would be suppressed after Aspirin treatment, without strict dose-effect. The cell apoptosis can be found after Aspirin treatment, as well as elevated ROS and reduced mitochondria membrane potential. The expression levels of relevant cytokines indicated down-reg- ulated NF-KB and up-regulated TNF-α, which may be the potential molecular mechanism for the tumor cell sup- pression effects of Aspirin. Cell migration with Transwell detection, The cells were treated with Aspirin and VB2 of different concentrations for 48 h （Table 2 and Figure 2 ）. Compared to the cell migration rate in control group （more than 80% ） , the cell migration was greatly reduced in both Aspirin and VB2 treated groups, which were both less than 40 %. Reactive oxygen, The reactive oxygen levels in Aspirin treated cells were greatly increased tobe 2-3 times compared to control group（Figure 3）. The dose-effect was not significant.
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