Radiation target and mutagenesis in intestinal tumors

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Attenuated expression of Bcl11b in Lgr5-expressing intestinal crypt cells promoted regeneration of intestinal epithelial cells after the radiation-induced injury in Lgr5-Cre; Bcl11bflox/+ mice. This suggests that the origin of cells in intestinal tumors, which are enhanced by loss of one Bcl11b allele in Apcmin/+ mice, is Lgr5-expressing cells. It was also demonstrated that Bcl11b functions as a subunit of SWI/SNF chromatin remodeling complex and down-regulates transcription of Wnt/beta-catenin target genes such as c-jun. This suggests that Bcl11b impairment instigates intestinal tumor development at least in part through deregulation of beta-catenin pathway.