OBJECTIVE: To examine the expression level of HOTAIR in pancreatic β cells. Moreover, regulatory effects of HOTAIR on insulin secretion, proliferation, cell cycle, and apoptosis in β cells are determined. MATERIALS AND METHODS: HOTAIR levels in mouse primary pancreatic cells and MIN6 cell line were determined by quantitative Real Time-Polymerase Chain Reaction (qRT-PCR). Its level was significantly observed in MIN6 cells treated with different doses of glucose. After the knockdown of HOTAIR, insulin secretion, cell cycle distribution, proliferation, and apoptosis in pancreatic β cells were assessed. RESULTS: HOTAIR was abundantly expressed in pancreatic islets. HOTAIR level in pancreatic tissues of db/db mice was downregulated and influenced by glucose level. Knockdown of HOTAIR attenuated insulin secretion and synthesis capacities in both MIN6 cells and primary pancreatic cells, which may be related by the downregulation of MafA, Pdx1, and NeuroD. Moreover, the silence of HOTAIR suppressed proliferation, arrested cell cycle, and stimulated apoptosis in pancreatic β cells. CONCLUSIONS: HOTAIR is highly expressed in pancreatic tissues. The silence of HOTAIR inhibits insulin secretion by downregulating insulin transcription-related genes. In addition, the silence of HOTAIR suppresses proliferation, arrests cell cycle progression, and induces apoptosis in pancreatic β cells.
OBJECTIVE: To examine the expression level of HOTAIR in pancreatic β cells. Moreover, regulatory effects of HOTAIR on insulin secretion, proliferation, cell cycle, and apoptosis in β cells are determined. MATERIALS AND METHODS:HOTAIR levels in mouse primary pancreatic cells and MIN6 cell line were determined by quantitative Real Time-Polymerase Chain Reaction (qRT-PCR). Its level was significantly observed in MIN6 cells treated with different doses of glucose. After the knockdown of HOTAIR, insulin secretion, cell cycle distribution, proliferation, and apoptosis in pancreatic β cells were assessed. RESULTS:HOTAIR was abundantly expressed in pancreatic islets. HOTAIR level in pancreatic tissues of db/db mice was downregulated and influenced by glucose level. Knockdown of HOTAIR attenuated insulin secretion and synthesis capacities in both MIN6 cells and primary pancreatic cells, which may be related by the downregulation of MafA, Pdx1, and NeuroD. Moreover, the silence of HOTAIR suppressed proliferation, arrested cell cycle, and stimulated apoptosis in pancreatic β cells. CONCLUSIONS:HOTAIR is highly expressed in pancreatic tissues. The silence of HOTAIR inhibits insulin secretion by downregulating insulin transcription-related genes. In addition, the silence of HOTAIR suppresses proliferation, arrests cell cycle progression, and induces apoptosis in pancreatic β cells.