Here we are the first time to show that CBX7 is overexpressed in gastric cancer cell lines and gastric cancer tissues; and stable knockdown of CBX7 expression in gastric cancer cells can induce cellular senescence, which constitutes a powerful barrier to oncogenesis [4], and inhibit proliferation in in vitro study. Importantly, we found that overexpression of CBX7 correlated with advanced clinical stage and positive lymph node metastasis. Our in vitro study also showed that knockdown of CBX7 expression inhibited the ability of migration in gastric cancer cells. This is the first time to find that CBX7 regulates cellular migration in in vitro model,

BMN-673 and provide preliminary direct evidence for the possibility of CBX7 regulating the metastasis of cancer. All these results suggest that CBX7 not only play important roles in tumorigenesis, but may also be involved in the progression and metastasis of gastric cancer. Our previous study showed that Bmi-1 was an independent negative prognosis factor

and patients with high Bmi-1 expression survived significantly shorter than those with low and no Bmi-1 expression [10]. In the present study, using the same patient Trametinib samples, we also found that patients with positive CBX7 expression survived significantly shorter than those with negative CBX7 expression. However, multivariate Cox proportional hazards model analysis showed that lymph node metastasis, AMP deaminase but not CBX7 is an independent prognosis factor. Collectively, our data suggest CBX7 shares similarities in functions with Bmi-1 in gastric cancer, but we didn’t confirm CBX7 is an independent prognosis factor as Bmi-1, which may be due to the limited samples in the present study, or the function of CBX7 may partially depend on Bmi-1, or its role is not as important as Bmi-1 in gastric cancer. It is interesting to note that the expression of CBX7 negatively

correlated with age in this study. The positive expression rate of CBX7 in old patients was significantly lower than that in young patients. As CBX7 is capable of regulating cellular proliferation and senescence [20], and CBX7 expression is downregulated during replicative senescence, the results suggest that cancer cells in aged person might have lower proliferative ability, or more cells in aged person are in the senescent state. It’s already known that CBX7 regulates cellular senescence and proliferation via Ink4a/Arf locus, which encodes the cyclin-dependent kinase inhibitor p16(INK4a) and tumor suppressor p19(Arf) [20]. However, what’s the down-stream target and mechanism of CBX7 during gastric carcinogenesis is still unclear. In the present study we found that knockdown of CBX7 resulted in increased p16(INK4a) expression and was accompanied by decreased transformed phenotype and migration ability, which suggested regulation of p16(INK4a) might be one of the important mechanisms of CBX7 in gastric cancer.