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Heterochromatin protein 1γ (CBX3) links histone methylation marks to transcriptional silence, DNA repair and RNA splicing, but a role for CBX3 in cancer remains largely unknown. In this study, we show that CBX3 in colon cancer cells promotes the progression of the cell cycle and proliferation in vitro and in vivo. Cell cycle (G1 phase to S phase) related gene CDK6 and p21 were further identified as targets of CBX3. In addition, we found that enhancing CDK6 suppresses cell proliferation by upregulating inhibitor p21 in the absence of CBX3, and this function is independent of the kinase activity of CDK6. Our results demonstrate a key role of CBX3 in colon carcinogenesis via suppressing the expression of CDK6/p21, which may disrupt the role of CDK6 in transcriptionally regulating p21, as part of a negative feedback loop to limit CDK6 excessive activation.

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Keloid is a type of pathological skin scar. Pathogenesis of keloid is complex and is not fully understood. lncRNA can regulate gene expression on different levels. It also participates in cell cycle regulation and cell proliferation. The present study investigated the potential biological function of lncRNA in keloid. We identified differential expression of lncRNAs and mRNAs between 3 pairs of keloid and normal skin tissue by microarray. Differentially expressed lncRNAs were validated by quantitative reverse transcriptase-PCR (qRT-PCR). Gene ontology (GO) and pathway analysis presented the characteristics of associated protein-coding genes. Additionally, a co-expression network of lncRNA and mRNA was constructed to find potential underlying regulation targets. There were 1,731 lncRNAs constantly upregulated and 782 downregulated, 1,079 mRNAs upregulated and 3,282 downregulated in keloid respectively (fold change ≥ 2.0, p<0.05). We chose, respectively, 3 upregulated and 1 downregulated lncRNA for qRT-PCR and results were consistent with microarray. Moreover, 11 pathways were related with upregulated transcripts and 44 with downregulated in keloid. The co-expression network revealed that one lncRNA was connected with numerous mRNAs, and vice versa. Furthermore, bioinformation analysis suggested that lncRNA CACNA1G-AS1 may be crucial to keloid formation. In conclusion, groups of lncRNAs were aberrantly expressed in keloid compared with normal skin tissue, which indicated that differentially expressed lncRNAs may play a key role in keloid formation. The present study provides new insights into keloid pathology and potential targets for treatment of keloid.

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