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Background  H3K9 trimethylation (H3K9me3) and binding of PcG repressor complex-1 (PRC1) may play crucial roles in the epigenetic silencing of the  p16  gene. However, the mechanism of the initiation of this trimethylation is unknown.    Methodology/Principal Findings  In the present study, we found that upregulating the expression of PRC1 component  Cbx7  in gastric cancer cell lines MGC803 and BGC823 led to significantly suppress the expression of genes within the  p16 - Arf-p15  locus. H3K9me3 formation was observed at the  p16  promoter and Regulatory Domain (RD). CBX7 and SUV39H2 binding to these regions were also detectable in the CBX7-stably upregulated cells. CBX7-SUV39H2 complexes were observed within nucleus in bimolecular fluorescence complementation assay (BiFC). Mutations of the chromodomain or deletion of Pc-box abolished the CBX7-binding and H3K9me3 formation, and thus partially repressed the function of CBX7. SiRNA-knockdown of  Suv39h2  blocked the repressive effect of CBX7 on  p16  transcription. Moreover, we found that expression of CBX7 in gastric carcinoma tissues with  p16  methylation was significantly lower than that in their corresponding normal tissues, which showed a negative correlation with transcription of  p16  in gastric mucosa.    Conclusion/Significance  These results demonstrated for the first time, to our knowledge, that CBX7 could initiate H3K9me3 formation at the  p16  promoter.

Polycomb CBX7 Directly Controls Trimethylation of Histone H3 at Lysine 9 at the p16 Locus