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CDH11  gene copy number and expression are frequently lost in human retinoblastomas and in retinoblastomas arising in TAg-RB mice. To determine the effect of  Cdh11  loss in tumorigenesis, we crossed  Cdh11  null mice with TAg-RB mice. Loss of  Cdh11  had no gross morphological effect on the developing retina of  Cdh11  knockout mice, but led to larger retinal volumes in mice crossed with TAg-RB mice (p = 0.01). Mice null for  Cdh11  presented with fewer TAg-positive cells at postnatal day 8 (PND8) (p = 0.01) and had fewer multifocal tumors at PND28 (p = 0.016), compared to mice with normal  Cdh11  alleles. However, tumor growth was faster in  Cdh11 -null mice between PND8 and PND84 (p = 0.003). In tumors of  Cdh11- null mice, cell death was decreased 5- to 10-fold (p<0.03 for all markers), while proliferation  in vivo  remained unaffected (p = 0.121). Activated caspase-3 was significantly decreased and β-catenin expression increased in  Cdh11  knockdown experiments  in vitro . These data suggest that  Cdh11  displays tumor suppressor properties  in vivo  and  in vitro  in murine retinoblastoma through promotion of cell death.

Cdh11 Acts as a Tumor Suppressor in a Murine Retinoblastoma Model by Facilitating Tumor Cell Death