Fig. 4

Details of CBX members regulate PI3K/AKT/mTOR, NF-κB signalling pathways in tumours and mechanism. (A) CBX2 could transcriptionally regulate PI3K/AKT signalling pathway activation in BC and GBM through classical PRC1-dependent pathway, playing a role in tumour promotion, other mechanisms might exist. In addition, it was found that CBX8 recognized H3K27me3 of downstream target genes in PC cells, but did not play a transcriptional inhibitory role, there were other ways to transcriptionally activate the expression of downstream target genes (the specific mechanism is still unclear) to regulate the activation of PI3K/AKT signalling pathway and play a role in tumour promotion. CBX3 has transcriptional activation in ccRCC/PCa (the specific mechanism is still unclear), which could increase the transcriptional activity of downstream target genes, regulate the activation of PI3K/AKT signalling pathway, and play a role in tumour promotion. In UBC, CBX7 could transcriptively silence the expression of downstream target genes in a classical PRC1-dependent manner, inhibit the activation of PI3K-AKT signalling pathway, play a role as a tumour-suppressive factor, and delay the malignant progression of tumours. (B) The transcriptional regulation mechanism of oncogenic factor CBX4 is involved in the regulation of NF-κB signalling pathway activation in NSCLC/OS cells. CBX6 could exert transcriptional activation independently of the classical PRC1-dependent pathway (the specific mechanism is not yet clear), upregulate the expression of downstream target genes, promote the activation of NF-κB signalling pathway in HCC, and play a role as a carcinogenic factor. Although CBX7 acts as a carcinogenic factor in GC, it could still play a transcriptional inhibitory role and promote the activation of NF-κB signalling pathway in GC, but the specific regulatory mechanism is unknown. CBX6 and CBX7 could inhibit the activation of NF-κB signalling pathway in BC/ccRCC cells by silencing the expression of downstream target genes through classical PRC1-dependent transcriptional pathway, thus acting as a tumour suppressor. CBX7 could transcribe and activate the expression of downstream target genes in PC cells independently of the classical PRC1-dependent pathway, and the NF-κB signalling pathway is activated to act as a tumour suppressor.