| Background and objective: The colorectal carcinoma is one of the mostcommon malignant neoplasms in the world, and its carcinogenesis and progression is a procedure involved of multigence and multiprocesure, including kinds of activation of proto-oncogences and inactivation of tumor suppressor genes. The fact that no significant improvements exit in the overall outcome for patients with colorectal carcinoma in recent years is mainly due to its recurrence and metastasis. Investigating the pathogenesis of colorectal rumor is very significant for the diagnosis, treatment, and prognosis of colorectal carcinoma. Recent studies have revealed that 3 -catenin gene(CTNNBl) is a proto-oncogene, and the protein of -catenin plays an important role in cell-cell adhesion and Wnt signaling pathway. It is involved into the procedure of carcinogenesis and progression of many kinds of neoplasms, and related to infiltration and metastasis closely; Protein kinase CPU (PKC P II ) is one of phospholipid-dependant serine/thersine protein kinases, which has functions in regulating growth, differentiation, and cell apoptosis. It is detected recently that the expression of PKC II in colorectal carcinoma increases aberrantly, but the pathogenesis that PKC II how to regulate -catenin ,and the relation between -catenin and colorectal carcinoma is not clarified, and there are few studies on the correlation of PKC 0 II to the characters of clinical pathology of colorectal carcinoma . This study evaluated the role of P -catenin, PKC P II in carcinogenesis and progression of colorectal carcinoma by immunohistochemistry method, in order to clarifmg the plausible mechanisms of carcinogenesis, progression, which may provides theoretic foundations for potential new therapy methods of colorectal carcinoma.Materials and methods: 69 colorectal carcinoma specimens, 21 adenomaand 16 normal mucosa specimens were collected. All tissues were identified by pathologist, fixed in neutral 10% formaldehyde, and embedded in paraffin. Immunohistochemical streptavidin peroxides(SP) conjugate method was used to analyze the expression of 3 -catenin, as well as PKC II, in normal colorectal mucosa, colorectal adenoma and colorectal carcinoma. Data were analyzed with SPSS 10.0 software. Chi-square test and fisher' exact test of probabilities were used, and Statistically significant level was considered as "alpha equals 0.05".Results:1. Expression of P -catenin protein:(l) Cytomembranous expression is normal expression. Aberrant expressions include reducing cytomembranous expression, cytoplasmic accumulation and nuclear translocation. (2) There were all positive staining in cytomembrane 16 colorectal normal mucosa samples, and the positive rate was 100%(16/16). The particles of positive staining distributed in the adherining site of cells, presenting as yellow or brown. But the aberrant expression was found incolorectal adenomas and colorectal carcinomas. The rate of P -catenin aberrant expression in adenomas and colorectal carcinomas was 57.14%(12/21),79.71%(55/69) respectively. The rate of P -catenin reducing expression in cytomembrane, cytoplasmic accumulation, and nuclear translocation expression was 19.05%(4/21), 57.14%(12/21),9.52%(2/21) in colorectal adenoma, but those were 44.93%(31/69), 69.57%(48/69),34.78%(24/69) in the colorectal carcinoma. Compared with adenomas and carcinomas in the same location, the difference of reducing expressionin cytomembrane of P -catenin was significant (P<0.05)between those two groups, as well as P -catenin nuclear translocation (P<0.05). But there was no difference in cytoplasmic accumulation (P>0.05).Besides, the aberrant expression of P -catenin in adenomas and carcinomas was significant comparing with the normal mucosa group (P<0.05);. (3) 69 colorectal carcinomas samples were divided into invasion within myometrium group and beyond myometrium group. Aberrant expression rate of P -catenin in those two groups showed ever-increasing tendency related to the infiltrated depth of carcinoma. |
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