Objective To review the research and del ivery methods of growth factors in tendon injuries, and to point out the problems at present as well as to predict the trend of development in this field. Methods Domestic and international l iterature concerning growth factors to enhance tendon and l igament heal ing in recent years was extensively reviewed and thoroughly analyzed. Results Cell growth factor could promote tendon heal ing, improve the mechanical properties as well as reduce the adhesion postoperatively. The use of transgenic technology mediating cell factors to promote tendon repair shows its advantages in many ways. Conclusion The growth factors play a vital role in tendon heal ing. Reasonable treatment of growth factors through direct appl ication or gene transfer techniques is of great value for the heal ing process.
Objective To explore the effect of interfering RNA (shRNA) on biological activity of A549 cells and tumor growth in nude mice after knockdown of estrogen receptor α (ERα) gene. Methods The ERα gene in A549 cells was knocked down by shRNA. RT-PCR and Western blot were used to detect the gene expression and protein expression after knockdown; colony formation experiment was used to detect the proliferation of cells, and RT-PCR was used to detect the expression of Ki-67 and PCNA; flow cytometry was used to detect apoptosis rate; transwell assay was used to detect cell invasion ability; Western blot was used to detect the expression of epithelial cadherin (E-cad) and neuropathic cadherin (N-cad) protein. The control group and A549 cells transfected with ERα-shRNA1 were injected subcutaneously in nude mice to construct transplanted tumors. Immunohistochemistry was used to detect the expression of Ki-67 and N-cad in tumor tissues. Results Compared with the control group, after transfection of ERα-shRNA1 and ERα-shRNA2, the mRNA and protein expressions of ERα were reduced significantly (P<0.05), and shRNA1 with high interference efficiency was used for subsequent experiments. Compared with the control group, the A549 cells were transfected with ERα-shRNA1, the colony formation rate was down-regulated significantly (P<0.05), the apoptosis rate was increased significantly (P<0.05), the expression of Ki-67 and PCNA were down-regulated significantly (P<0.05), the number of invasive cells was reduced significantly, the expression of E-cad was increased, and the expression of N-cad was decreased (P<0.05). The results of tumor formation in nude mice showed that interfering with ERα expression can significantly inhibit tumor growth (P<0.05), and down-regulate the rate of Ki-67 and N-cad positive cells (P<0.05). Conclusion Knockdown of ERα inhibits the proliferation and migration ability of NSCLC cells and the occurrence and development of transplanted tumors in nude mice.