Disease relevance of CBX7

• CBX7 was expressed at high levels in germinal center lymphocytes and germinal center-derived follicular lymphomas, where elevated expression correlated with high c-Myc expression and a more advanced tumor grade [1].
• CBX7 was highly expressed in three different prostate cancer cell lines and present at elevated levels in normal prostate [2].
• By targeting Cbx7 expression to the lymphoid compartment in mice, we showed that Cbx7 can initiate T cell lymphomagenesis and cooperate with c-Myc to produce highly aggressive B cell lymphomas [1].

High impact information on CBX7

• CBX7 does not inter-function or colocalize with Bmi1, and both can exert their actions independently of each other as shown by reverse genetics [3].
• In a genetic screen for cDNAs bypassing replicative senescence of normal human prostate epithelial cells (HPrEC), we identified CBX7, a gene that encodes a Polycomb protein, as shown by sequence homology, its interaction with Ring1 and its localization to nuclear Polycomb bodies [3].
• These data identify CBX7 as a chromobox protein causally linked to cancer development and may help explain the low frequency of INK4a/ARF mutations observed in human follicular lymphoma [1].
• CBX7 knockdown caused an impairment of cell growth that was dependent on the status of the p14Arf/p53 and p16Ink4a/Rb pathways in both normal and cancer prostate cells [2].
• In an attempt to identify a putative role of CBX7 in tumorigenesis, we analysed CBX7 expression in a panel of cancer cell lines and primary tissues [2].

Biological context of CBX7

• Ablation of CBX7 expression using short hairpin RNAs (shRNA) resulted in upregulation of p16Ink4a and p14Arf in both LNCaP and PC-3 prostate cell lines [2].

Associations of CBX7 with chemical compounds

• CBX7 overexpression in LNCaP cells resulted in a slight growth advantage in both androgen-dependent and -independent conditions [2].

References