Silenced DMBT1 promotes nasal mucosa epithelial cell growth.

ObjectiveThe aim of this study was to investigate the role of the deleted in malignant brain tumors 1 (DMBT1) gene in the development of nasal polyps, as well as related mechanisms. MethodsA stable human nasal mucosa epithelial cell (HNEpC) line with low expression of DMBT1 was generated. Three groups were established: a control group (HNEpCs without any treatment), a control short interference RNA (shRNA) group (HNEpCs transfected with an empty vector), and a DMBT1 shRNA group (HNEpCs with silenced DMBT1). Cell viability, apoptosis, and cell cycle distribution were measured after incubation. Expression of p53, signal transducer and activator of transcription 3 (STAT3), protein kinase B (AKT) and extracellular signal-regulated kinase1/2 (ERK1/2) was detected by western blotting. ResultsCompared with the control cell line, HNEpCs with silenced DMBT1 had increased viability and decreased apoptosis. Moreover, after DMBT1 silence, cell numbers were decreased significantly in the G1 phase and increased in the G2 and S phases. DMBT1 silence was associated with increased AKT expression and decreased p53 expression, but it did not alter expression of ERK1/2 or STAT3 (P>0.05). Compared with the control cell line, HNEpCs transfected with an empty vector did not have altered cell viability, apoptosis, cell cycle distribution or expression of AKT, p53, ERK1/2, or STAT3 (P>0.05). ConclusionDMBT1 plays an important role in the growth and division of nasal epithelial cells. The possible mechanism might involve DMBT1 regulating the AKT-p53 pathway to promote cell viability and reduce apoptosis of nasal epithelial cells.