Fig. 3

Details of CBX members regulate Wnt/β-catenin, Hippo, MARK signalling pathways in tumours and mechanism. (A) CBX1 and CBX3, respectively, play a transcriptional activation role in HCC and CRC (the specific mechanism of action is not yet clear), could upregulate the expression of downstream target genes to promote the activation of Wnt/β-catenin signalling pathway and play a tumour promotion role. However, it is not clear CBX2/4/8 through what transcriptional regulatory mechanism overactivates the Wnt/β-catenin signalling pathway in GC/LUAD/LSCC cells to play the role of carcinogenic factors. CBX7 could act as a methylation reader to identify H3K27me3 on the promoter of downstream target genes, silence the expression of downstream target genes through classical PRC1-dependent transcriptional pathway, inhibiting the activation of Wnt/β-catenin signalling pathway, and act as a cancer suppressor. However, although CBX7 also exists as a tumour suppressor in BC cells, it exerts transcriptional activation independently of the classical PRC1-dependent pathway, upregulates the expression of downstream target genes, and inhibits the activation of Wnt/β-catenin signalling pathway. (B) CBX2 in HCC might be independent of the classical PRC1-dependent pathway, playing a role in transcriptional activation (the specific mechanism is not clear), upregulating the expression of downstream target genes, inhibiting the activation of Hippo signalling pathway, and playing a role in tumour promotion. However, the transcriptional regulatory mechanism of oncogenic factor CBX4 in inhibiting Hippo signalling pathway activation in LUAD cells in the context of KrasG12D mutation remains unclear. In GBM, CBX7 could inhibit the expression of downstream target genes through classical PRC1-dependent pathway transcription, promote the activation of tumour suppression-related Hippo signalling pathway, inhibit the activation of EMT-related SAPK/JNK signalling pathway, and play a role as a cancer suppressor, which is conducive to patients' prognosis. CBX2 could inhibit the expression of downstream target genes through classical PRC1-dependent pathway transcription, promote the activation of MAPK signalling pathway in AML, and play a role as a carcinogenic factor. Although CBX8 could recognize H3K27me3 in HCC cells, it transcriptionally activating the expression of downstream target genes through other mechanisms independent of the classical PRC1-dependent pathway, promoting the activation of MAPK signalling pathway, and playing a role as a carcinogenic factor. The transcriptional regulation mechanism of oncogenic factor CBX7 in promoting the activation of MAPK signalling pathway in OC cells remains unclear. CBX7 could silence the expression of downstream target genes through classical PRC1-dependent transcriptional pathway, inhibit the activation of MAPK signalling pathway in UBC, and act as a tumour-suppressive factor. However, it is not clear whether the transcriptional regulation mechanism of CBX7 is involved in the regulation of ERK/MAPK signalling pathway activation in NSCLC cells.