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1.
Journal of Medical Postgraduates ; (12): 1169-1173, 2019.
Article in Chinese | WPRIM | ID: wpr-818161

ABSTRACT

Objective MicroRNA-145 (miR-145) is underexpressed in breast cancer. The study aimed to explore the regulatory effect of miR-145 on breast cancer MCF-7 cells by investigating the association of miR-145 with ADAM17 and EGFR. Methods The MCF-7 breast cancer cells were divided into three groups: the transfection group (transfected with microRNA-145 mimics), the control group (without transfection) and the nonsense sequence group (transfected with nonsense microRNA). MTT, transwell and real-time quantitative fluorescence polymerase chain reaction(qPCR) were respectively used to detect the proliferative capacity, invasive ability and expression of MCF-7 breast cancer cells after the transfection of miR-145 in three groups. ADAM17 and EGFR mRNA and protein levels in three groups of breast cancer MCF-7 cells were detected by qPCR and western blot. Results The results of qPCR showed that the relative expression of miR-145 was significantly higher in transfection group (13964.33±1265.30) than those in control group (1.00±0.05) and nonsense sequence group (1.03±0.15) and the difference was statistically significant (P<0.01); the expression of ADAM17 mRNA in transfection group (1.71±0.08) was significantly higher than that in control group (1.00±0.07) and the difference was statistically significant (P<0.01). Compared with the nonsense sequences at 24 h, 48 h, and 72 h, the inhibition rate of MCF-7 in transfection group was significantly increased (P<0.01). The results of transwell invasion showed that the number of transmembrane cells in transfection group [(56.20±2.17)/field] was significantly lower than those in control group [(92.80±3.90)/field] and nonsense sequence group [(91.80±4.97)/field of view ] (P < 0.01). Western blot results showed that the protein content of ADAM17 and EGFR in transfection group was significantly lower than those in the control group and the nonsense sequence group (P<0.01). Conclusion MiR-145 inhibits the proliferation and invasion of breast cancer MCF-7 cell line by acting on the ADAM17-EGFR signaling pathway.

2.
Chinese Journal of Integrated Traditional and Western Medicine ; (12): 1122-1126, 2011.
Article in Chinese | WPRIM | ID: wpr-299058

ABSTRACT

<p><b>OBJECTIVE</b>To study the feasibility of repairing bone defect by combined autologous bone marrow transplantation, cuttebone, and sodium hyaluronate.</p><p><b>METHODS</b>Forty-eight New Zealand rabbits were randomly divided into four groups. The 10-mm bone defect of the radial shaft animal model was established, with the periosteum remained. Rabbits of Group A were treated by autologous bone marrow transplantation, cuttlebone, and sodium hyaluronate. Those of Group B were treated by autologous bone marrow transplantation and cuttlebone. Rabbits of Group C were implanted with cuttlebone and sodium hyaluronate. And rabbits of Group D were taken as the blank control. There were twelve rabbits in each group. All rabbits were sacrificed, and the general histological examination, X-ray test, the pathohistological observation and scoring, the new born formation area measurement were performed at 2-week, 4-week, 8-week, and 12-week after transplantation respectively. The capacities for bone transplantation and defect repairing were compared and analyzed as well.</p><p><b>RESULTS</b>The bone defect of Group A was completely repaired at week 12. The comprehensive indices at each time point were superior to those of the rest groups, showing statistical significance (P<0.05). The bone repair in Group B and Group C were somewhat poor, with the repairing effect inferior to that of Group A. The bone repairing was better in Group B than in Group C. Most portion of the bone defect in Group D was filled with fibrous tissue and muscular tissue, with little bone repairing.</p><p><b>CONCLUSIONS</b>The combined autologous bone marrow transplantation, cuttlebone, and sodium hyaluronate showed obviously synergistically bone forming capacities. It could be taken as a substitute material for transplantation.</p>


Subject(s)
Animals , Rabbits , Bone Marrow Transplantation , Bone Regeneration , Bone Substitutes , Bone and Bones , Wounds and Injuries , Drugs, Chinese Herbal , Therapeutic Uses , Hyaluronic Acid , Therapeutic Uses , Transplantation, Autologous
3.
Chinese Journal of Industrial Hygiene and Occupational Diseases ; (12): 468-471, 2008.
Article in Chinese | WPRIM | ID: wpr-315664

ABSTRACT

<p><b>OBJECTIVE</b>To study the effect of silicosis alveolar macrophages (AM) restimulated by SiO(2) on expression of c-myc oncogene in human embryo lung fibroblasts.</p><p><b>METHODS</b>The bronchoalveolar lavage of silicosis patients was collected. AMs were divided into 2 groups: (1) SiO(2): AMs were stimulated with SiO(2) (30 microg/ml) for 1, 2, 6, 12, 24 and 36 h; (2) control: treated for the same time without SiO(2). Fibroblasts were cultured with different AMs supernatants for 2 h or 7 h respectively. The expression of c-myc mRNA was determined by RT-PCR and protein by Western Blot.</p><p><b>RESULTS</b>There was no c-myc expression when fibroblasts were static. The supernatants in the S6 group stimulated expression of c-myc mRNA and protein, with the peak expression at 2 h and 7 h respectively. In the control group, AMs supernatants cultured in different time stimulated expression of c-myc mRNA and protein with the most evident expression at 12 h. The ratios were 0.749 +/- 0.088 and 0.759 +/- 0.101 respectively. Compared with control in the same period, c-myc mRNA and protein expression were significantly stronger treated with the supernatants in which AMs were stimulated for 1 h, 2 h and 6 h by SiO(2) (P < 0.05 or P < 0.01).</p><p><b>CONCLUSION</b>AMs stimulated with SiO(2) has the ability to induce c-myc oncogene expression in human embryo lung fibroblasts.</p>


Subject(s)
Humans , Cells, Cultured , Fibroblasts , Metabolism , Lung , Metabolism , Pathology , Macrophages, Alveolar , Metabolism , Proto-Oncogene Proteins c-myc , Genetics , Metabolism , RNA, Messenger , Genetics , Silicon Dioxide , Toxicity , Silicosis , Metabolism , Pathology
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