Study Of Relationship Between CatB And P53 Expressions And Malignancy In Human Glioma

Glioma from the interstitial cells of neural origin, took place in neuroectodermal tumor, neuroectodermal tumor, or it is also known as neuroepithelial tumors。The incidence of glioma brain tumors account for 40 to 50%, is the most common intracranial tumors, mostly malignant tumors. The treatment of multiple treated by operation, the tumor showed infiltrative growth, with no clear boundaries in brain tissue, Nanyichedi excision, Shu Hou should Radiation Therapy, chemotherapy, immune therapy [1]. Cat (Cathepsin) is a lysosomal protein dissolving enzyme, physiological conditions, only play a role in the lysosome; in tumor tissues, Cat can degrade proteoglycans, LN (fibronection, FN), FN (laminin) and type IV collagen and other extracellular matrix components, Cat also by activating other protein degradation in the original collagenase enzymes and indirectly involved in extracellular matrix degradation. Matrix degradation through the promotion of tumor cell proliferation involved in the process of tumor invasion [2]. Another study pointed out that the Cat could promote proliferation of tumor blood vessels, and Cat transcription, the level of expression and the tumor was positively correlated with the prognosis [3]. P53 gene in human tumor suppressor gene. The gene codes for a molecular weight of 53kDa protein, named P53. P53 gene inactivation plays an important role in tumor formation. But the thing is bound to two aspects of it, P53 is an important anti-cancer genes to cancer cells commit suicide, to prevent cancer; also has to help cells repair gene defects in the function. This feature is injured by the chemotherapy drugs and cancer cells, then from the repair, rather than to cancer cells commit suicide. Cause cancer cells to be repaired after treatment, a new tumor.P53 gene is found in human tumors so far, the most relevant genes. In just over a decade, people's understanding of the P53 gene experienced a cancer antigen, tumor suppressor genes in cancer gene to change the three knowledge has been recognized caused tumor formation or cell transformation of P53 protein is a product of P53 gene mutation is a tumor promoting factor, which can eliminate the normal function of P53, while the wild-type P53 gene is a tumor suppressor gene, its inactivation of tumor play an important role in the formation. P53 protein was mainly concentrated in nucleolar areas, specific binding with DNA, and its activity regulated by phosphorylation. Normal biological function of P53 is like genome guardian (guardian of the genome), in the G1 phase DNA damage check points to monitor the integrity of the genome. If injury, P53 protein prevents DNA replication in order to provide sufficient time to repair DNA damage; If repair fails, P53 protein was induced apoptosis; If the P53 gene mutations in both copies, out of control on cell proliferation, leading to carcinogenesis.Objective This method of immunohistochemistry in 60 cases of glioma expression of CatB and P53 to investigate its role in the development of glioma, as the judge of tumors and the diagnosis and treatment of new ideas and new methods.Methods(1) Using immunohistochemistry (Streptavidin.peroxidasebio.tin), were detected in 49 cases of glioma CatB, P53 protein expression and analysis in glioma CatB, P53 protein expression and clinicopathological characteristics relationship and the correlation between them.(2) CatB, P53 protein detection methods:CatB, P53 protein in cells in specific parts of the two indicators appear brown granules, staining intensity was higher than the background non-specific staining positive cells, positive cells reported in the literature to judge the standard reference to semi-quantitative method.(3) Using statistical software SPSS 15.0 statistical analysis of the data.Results (1) Five cases of cerebral hemorrhage due to hypertensive intracranial decompression of normal brain tissue CatB, P53 protein was negative.(2) 51 cases of glioma in 40 cases of CatB expression, the positive rate was 78.43%;Ⅰlevel in 15 cases,9 cases of positive expression, the positive rate was 60%;Ⅱlevel in 11 cases, eight cases of positive expression, positive expression rate to 72.73%;Ⅲgrade 12 cases,10 cases of positive expression, positive expression rate of 83.33%;Ⅳ,13 cases,13 cases of positive expression, positive expression rate of 100%, the difference was statistically significant (P<0.05), with pathological higher level gradually increased, different grade gliomas differences between groups were statistically significant (P<0.05). The CatB expression and patient age, sex and tumor location, size, shape independent (P> 0.05).(3) A total of 51 cases of 23 patients with glioma tumor expression of P53 protein, the positive rate was 45.09%; I level in 15 cases, two cases of positive expression, the positive rate was 13.33%; II level in 11 cases,3 cases of positive expression, positive expression rate was 27.27%; III grade 12 cases, eight cases of positive expression, positive expression rate of 66.67%; IV grade 13 cases,10 cases of positive expression, positive expression rate of 76.92%. Gliomas of different levels, P53 protein expression in different, the difference was significant (H=18.021, P<0.01). In the high-level (Ⅲ,Ⅳgrade) glioma P53 protein expression was significantly higher than the low-level (I, II grade) gliomas (P<0.05). P53 protein expression in glioma tumor intensity into rank correlation (r_s= 0.556, P<0.01).Conclusion(1) Normal brain tissue without CatB and P53 protein expression.(2) CatB glioma in the high-level (Ⅲ～Ⅳ) group was significantly higher than expression in gliomas of low-level (Ⅰ,Ⅱ) group of gliomas, indicating CatB associated with malignant glioma.(3) P53 protein expression and the level of expression associated with cancer, P53 protein overexpression is a high malignant, poorly differentiated biological characteristics of glioma. (4) CatB and P53 protein in human gliomas suggest a positive correlation between expression in glioma genesis and development of cooperative or mutual regulation plays a role in the invasive growth of human glioma cells and malignant play an important role in the development. It can serve as a prognostic and monitoring indicators of tumor recurrence or metastasis has some clinical significance. By inhibitors, may also be provided for the glioma after a new therapeutic approach.