Experimental Studies On Proliferation And P27 Expression Of Hypertrophic Scar Fibroblasts By C-myc Antisense Oligonucleotide

Background: Hypertrophic scar (HS), characterized by excessive fibroblast proliferation and local collagen deposition, is a very common pathologic phenomenon of scar hyperplasia after human skin injury and wound healing, and its pathogenesis is still unclear. Hypertrophic scar and scar over-contracture often destroy patient's cosmetics or result in patient's dysfunction of organs. Up to now, there is no effective method to treat scar. With the development in molecular techniques, gene therapy is reported as a hopeful way to treat many diseases. In theory, gene therapy may prevent many kinds of diseases from emerging or developing. The key point for gene therapy is how to select target gene and target cell. Proto-oncogene c-myc encodes a nuclear 62KD phosphorprotein, which acts as a key regulator of cell growth and differentiation. When dimerized with its partner protein Max, c-myc functions as transcription factor, capable of both activating and repressing transcription. C-myc is an eternal oncogene and plays a critical role in regulating cell proliferation, growth, apoptosis and differentiation. Over expression of c-myc is one of the most common alterations in human cancers. Recent years, foreign studies have identified that c-myc oncogene is closely related to hypertrophic scar. Some researchers have found that, by use of flow cytometry and Western Blotting, the level of c-Myc protein in tumor cells significantly reduces after transfection by c-myc ASODN. The early period of hypertrophic scar formation might be a good time for preventing overgrowth and contraction of hypertrophic scar by gene therapy. However, whether c-myc ASODN can cause the reduction of c-myc mRNA expression in fibroblasts is unknown.p27 is a member of the universal cyclin-dependent kinase inhibitor...