Table VII.

CBXs regulating malignant phenotype changes in tumors through posttranslational modifications.

Cancer type	Malignant phenotype changes	Regulation mechanism	(Refs.)
HCC	Proliferation; apoptosis	CBX2 knockdown inhibits the expression of WTIP, stimulates the Hippo pathway, and leads to the phosphorylation-induced inactivation of YAP	(212)
Glioma	Proliferation; tumorigenesis	CBX3 directly suppresses PARK2 and STUB1 at the transcriptional level to reduce the ubiquitination of EGFR	(213)
HCC	Angiogenesis	CBX4 promotes HCC via HIF-1α ubiquitination and VEGF upregulation	(214)
BC	EMT	Increased SENP7L decreases the SUMOylation of CBX5	(215)
BC	Chemosensitivity	Ubiquitinated CBX5 is recruited to ncRNA-rich chromatin loci to promote DNA damage and is associated with chemosensitivity in BC mediated via SUMOylated CBX5/ncRNA	(216)
EC	Proliferation; radiosensitivity	The inhibition of CBX8 increases the phosphorylation of p21, Wee1 and choline kinase 1	(90)

CBX, chromobox; HCC, hepatocellular carcinoma; BC, breast cancer; EC, esophageal cancer; EMT, epithelial to mesenchymal transition; WTIP, Wilms' tumor protein 1-interacting protein; YAP, Yes-associated protein; PARK2, Parkinson disease 2; STUB1, stress induced phosphoprotein 1 homology and U-box containing protein 1; EGFR, epidermal growth factor receptor; HIF-1α, hypoxia-inducible factor-1α; VEGF, vascular endothelial growth factor; SENP7L, SUMO specific peptidase 7 long transcript; SUMOylation, small ubiquitin-like modifier.