Objective To investigate the effect of miR-145 on human lung adenocarcinaoma A549 cell proliferation and FSCN1 expression. Methods pmR-mcherry/miR-145 was constructed and transfected into A549 cell,then the expression of miR-145 and the proliferation of A549 cell were verified by QPCR and MTS assay, respectively.The situation of FSCN1 expression in A549 cell was detected by Western blot.Results pmR-mcherry/miR-145 vector was constructed successfully,and QPCR results indicated that miR-145 expressed effectively.Western blot results showed that FSCN1 was one of the targets of miR-145 in A549 cell.MTS assay results indicated that miR-145 inhibited the proliferation of A549 cell.Conclusion Overexpression of miR-145 can inhibit the proliferation of A549 cell, and FSCN1 was one of its target.

BACKGROUND:Tissue-engineered biomaterials have the similar structure and function with autologous tissues. OBJECTIVE:To explore the osteoinduction of the bone biomaterial composited with rat bone marrow mesenchymal stem cel s in the treatment of large costal defects. METHODS:Forty Wistar rats were enrol ed used for the preparation of right large costal defect models, and then randomized into two groups, fol owed by the implantation of calcium chloride-sodium alginate gel (control group) or chloride-sodium alginate-bone marrow mesenchymal stem cel s (experimental group). At 2, 4 and 8 weeks after implantation, chest X-ray radiograph and histological examination of the defect region were conducted. RESULTS AND CONCLUSION:X-ray showed that in the experimental group, the defect area had no significant changes at the 2nd week after implantation until the formation of few bones at the 4th week;and at the 8th week, both ends of the defect region gradual y connected, and newly formed bones were ful of the defect. In contrast, the defect region in the control group showed no obvious bone healing, and both ends of the defect closed and osteosclerosis occurred. In the experimental group, there were a smal amount of fibrous tissues and numerous inflammatory cel s infiltratied in the material compartment, and no connection occured between the material and broken ends;there were numerous inflammatory cel s but no bone tissues in the control group at the 2nd week. At the 4th week, the scaffold degraded gradual y and abundant bone tissues were seen in the experimental group;the scaffold degraded little, and bone tissues aggregatied at the both defect ends in the control group. Up to the 8th week, the two kinds of scaffolds degraded mostly. A large number of bone tissues and trabeculae formed and the both defect ends were connected with the newly formed bones in the experimental groups, while in the control group, osteosclerosis appeared at both ends of the defect. To conclude, the bone biomaterial composited with rat bone marrow mesenchymal stem cel s promotes the repair of large costal defects.