Disruption of Smad4 in odontoblasts and dental epithelial cells influences the phenotype of multiple keratocystic odontogenic tumors.
作者： Weipeng Jiang , Guan Yang , Feng Chen , Xiao Yang , Tiejun Li
DOI: 10.1016/J.BBRC.2015.05.051
关键词:
摘要: Keratocystic odontogenic tumors (KCOTs) are cystic epithelial neoplasms with a high recurrence rate. The molecular mechanisms underlying the initiation and progression of KCOTs still largely unknown. Previous research showed that specific ablation Smad4 in odontoblasts dental epithelia resulted spontaneous mice, constitutively activated Hedgehog (Hh) signaling was detected cyst both Smad4Co/Co OC-Cre K5-Cre mice. Here, we ablated mouse compared sizes numbers KCOTs. Both number size mice were larger than those suggesting paracrine signals from root play more important role Hertwig's sheath (HERS) cells.
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