Peripheral nerve injuries represent a great challenge for surgeons. The conductive neural scaffold has experienced increasing interest because of its good biocompatibility and similar electrical properties as compared to those of a normal nerve. Herein, nerve conduits made from poly(d,l-lactide)-co-poly(ethylene glycol) and polypyrrole (20%, 30%, and 50%) (PELA–PPY) were prepared by electrospinning, and used in regeneration of peripheral nerve defects. The results of an in vitro experiment indicated a high biocompatibility for the as-prepared materials, supporting the attachment and proliferation of a rat pheochromocytoma PC-12 cell. Furthermore, the PELA–PPY nerve conduit implanted in the sciatic nerve defects (10 mm) of the Spraguee–Dawley rats for 12 weeks showed similar results with the autograft, while it demonstrated a better outcome than the PELA nerve conduit in electrophysiological examination, sciatic function index, total amount of regenerated myelinated nerve fibers, axon diameter, myelin thickness, and several immunohistochemistry indices (S-100, laminin, neurofilament, bromodeoxyuridine, and glial fibrillary acidic portein). We supposed that the bioactivity is mainly generated by the PPY in composite nanofibers which could transmit self-originated electrical stimulation between cells. Due to the facile preparation and excellent in vivo performance, the PPY–PELA nerve conduit is promising for use as a bioengineered biomaterial for peripheral nerve regeneration.
BackgroundWhile many studies have shown that levels of miR-26a are lower in papillary thyroid carcinoma (PTC), the role and mechanism of miR-26a in PTC are unclear.MethodWe used database searches to select potential mRNA targets of miR-26a. Anti-miR-26a, miR-26a mimic, siRNA for CKS2 and their effects on cell growth, cell-cycle distribution and colony formation were evaluated. We also evaluate the over-expressed miR-26a in TPC-1 cells in severe combined immune-deficient mice. We used luciferase reporter assays, real-time PCR and western blot analysis to measure the expression and activity of miR-26a, CKS2, and related factors such as cyclin B1, cyclin A, cdk1, bcl-xl and Akt. Finally, we measured the relationship between the levels of miR-26a and CKS2 in PTC and normal thyroid tissues.ResultsRelative to normal thyroid tissues, miR-26a is consistently down-regulated in TPC specimens, and CKS2 was identified as a potential target. Up-regulated miR-26a expression or down-regulated CKS2 expression in TPC-1 and CGTH W3 cells lines caused G2 phase-arrest. Decreased miR-26a expression or increased CKS2 expression could have inverse function on PTC cell lines. CyclinB1, cyclinA, bcl-xl and AKt are indirectly regulated by miR-26a in a CKS2-dependent manner. Finally, CKS2 is overexpressed in PTC specimens relative to normal thyroid tissue, and a significant inverse correlation exists between miR-26a and CKS2 expression in clinical PTC specimens.ConclusionOur data indicate that miR-26a functions as a growth-suppressive miRNA in PTC, and that its suppressive effects are mediated mainly by repressing CKS2 expression.
Abstract. Src is a tyrosine kinase that is of significance in tumor biology. The present review focuses on Src, its molecular structure, and role in cancer, in addition to its expression and function in sarcoma. In addition, the feasibility of Src as a potential drug target for the treatment of sarcoma is also discussed. Previous studies have suggested that Src has essential functions in cell proliferation, apoptosis, invasion, metastasis and the tumor microenvironment. Thus, it may be a potential target for cancer therapy. Src has been found to enhance proliferation, reduce apoptosis and promote metastasis in certain subtypes of sarcoma, including osteosarcoma, chondrosarcoma and Ewing's sarcoma. Furthermore, a number of novel effective therapeutic agents, such as SI-83, which target Src have been investigated in vitro and in vivo. Bosutinib and dasatinib, which inhibit Src, have been approved by the U.S. Food and Drug Administration for the treatment of chronic myelogenous leukemia. In addition, vandetanib is approved for the treatment of medullary thyroid cancer. Furthermore, the Src inhibitor, saracatinib, is currently in clinical trials for the treatment of a variety of solid tumors, including breast and lung cancers. Thus, Src is considered to be an important factor in sarcoma progression and may present a novel clinical therapeutic target. This review demonstrates the importance and clinical relevance of Src in sarcoma, and discusses a number of small molecular inhibitors of src kinase, such as dasatinib and sarcatinib, which are currently in clinical trials for the treatment of sarcoma patients.
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