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TPG TGP on Bcl-2,[link widoczny dla zalogowanych], c-myc gene expression and induction of apoptosis mechanisms


± 7.8l549.842 ± 6.4291) 2) 57.760 ± 7.6821) 54.152 ± 8.6101) 2) Note: 1) P <O. 01vsmodelgroup; 2) P <O. 05vsCINgroup3 discuss the apoptosis signal transduction is the general process: internal and external apoptotic cells integrate various cellular signals, apoptotic signal through its receptor complex formed by the cytoplasmic signal transduction protein is passed to the implementation of a group of cells by caspases, caspases then activate the degradation of its specific substrate, eventually leading to apoptosis. This experiment showed that by flow cytometry, 1, GC tumor-bearing mice can promote apoptosis of tumor cells, apoptosis occurred early peak, the peak increased, and the induction of apoptosis in the cell cycle phase and S phase C1. TCC induced apoptosis in tumor cells, apoptosis cycle in C1 and S phase of the apoptotic rate was 17.26%. Observed from the electron micrograph, TCC effect, the tumor cells and the nuclear membrane shrinkage, fracture, indicating that the drug has a direct effect on tumor cells in vitro. The experimental model mice Bc1.2 Yang States Journal of Immunology 2005 volume of the detection of more than 2l TCC group and the CTX group (P <0.05), suggest TCC tumor cells on Bcl-2 protein expression regulation, decreased expression of Bcl-2 protein can induce cell differentiation. Inhibitor of apoptosis (Apoptosisoff) gene Bcl-2 family has been taken seriously. Bc1.2 gene encoding the product of Bcl-2 protein can be wild-type p53 protein by blocking apoptosis and inhibition of apoptosis induced by a variety of factors involved in cell proliferation and apoptosis in the regulation of homeostasis. Abnormal expression of Bcl-2 gene can increase the genetic abnormality has been altered cells escape apoptosis, leading to cell transformation as well as tumor formation J. Oncogene c. myc is a slow reaction of immediate early response gene, to maintain the dynamic balance of cell proliferation and apoptosis, induced cell transformation and tumor formation. The protein encoded by c-myc is an important eukaryotic cells transcription factor, can induce transcription of the downstream reporter gene mRNA and protein expression in malignant tumors, tumor cell proliferation and apoptosis levels of cell proliferation and apoptosis regulation. c-myc is a major genetic regulation of cell cycle, and its overexpression can shorten the cell cycle, split to increase, but also increased cell apoptosis. The N-terminal protein binding with the PRB Erzhi which loss of function of tumor suppressor, so that the growth of tumor cells to achieve significant advantages. cmyc activity expression of p-catenin / TCF-4 complex, to regulate the primary and tumor-related signaling pathways Hh / Wnt pathway. This study demonstrates that the model group c-myc expression was strongly positive, with the TGC and the CTX group had significant difference. TCC group reduced c-myc expression, indicating that TGC can inhibit the expression of c-myc to promote apoptosis and inhibit tumor cell proliferation and production functions. Conclusion that TGC can induce apoptosis, and demonstrate the molecular mechanism of the effect c. myc, Bcl-2 expression and inhibit malignant cell proliferation, induce apoptosis, promote differentiation, with significant antitumor effect. 4
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