| In the present research on molecular oncology, studies on signal transduction, apoptosis, adhesion of cells, vasculogenesis, and telomerase activity become intensively noticed. The molecule, protein kinase C (PKC) , is involved in all these processes.PKC, a phosphatide-dependent calcium-activated Ser/Thr protein kinase, is a multiple genes-encoded superfamily of isoenzymes, which is consist of at least 13 isoformes. Based on dependence of calcium and DAG, PKC is generally grouped into 3 groupes: (1) classical PKC: isoforme a, βI, βII, and - β;(2) no-vel PKC:and 6; (3) atypical PKC: T/X,nd PKC-3. Moreover, there are PKC, and PRK. Each isoforme is structurally similar. PKC exists in almost all tissues of animals. Since each isoforme has different characteristics, expression, localization, and function, PKC is considered heterogenous. PKC is not only key to intracellular signal transduction, but also direcdy phosphorylates many critical proteins, so as to play complex roles. Through the regulation on telomerase, p21ras Bcl-2, MAPK/ERK, MMPs, VEGF, and adhesive molecules , PKC is involved distincdy in the complicated biological behavior of neoplasm.Ameloblastoma (AB) is the most frequendy occuring odontogenic tumor, its frequency is 59.3% in China. AB is regarded as a benign tumor by WHO. However, it may progressively invade the jaw, recure locally and transform ma-lignandy. AB is therefore considered semi-malignant. Odontogenic keratocyst ( OKC) is something similar to AB. We detected expression of protein kinase C-a in AB and OKC, and analyzed the correlation to investigate the molecularmechanism in the regulation of telomerase, and study the relation between cell differentiation and its clinical biological behavior in AB to provide some theoretic bases for diagnosis, therapy and prognosis of AB.Materials and methodsThe specimens used in immunohistochemistry were surgically removed from 54 patients with AB (primary AB 31 cases, recurrent AB 19 cases, malignant AB 4 cases) , 16 patients with OKC, and 7 patients with normal oral mucosa at the First Affiliated Hospital of China Medical University between 1987 ~2001. We detected PKC by SABC method. We used a scoring system to evaluate the immunoexpression semiquantitively. SPSS for 11.5 statistical software was used to solve the data. Chi-square test was used to analyze the correlation . The probability of P <0.05 was regarded as statistically significant.ResultPKC-a expresses in normal oral mucosa epithelium with a positive rate as 57.1% (4/7) and a strongly positive rate as 28.9% (2/7) , while those in OKC are individually 56.2% (9/16) and 31.2% (5/16). In AB, they are 85. 1% (46/54) and 72.2% (39/54) , in which 16 cases present nuclear posi-tivity as 29. 6% (16/54). Positive expression is also found within fibroblasts, vascular endothelial cells, and inflammatory cells in AB. The difference among AB, OKC, and normal epithelium is significant ( x =11. 725, P =0. 003). The positive rate is 58.0% (18/31) in primary AB, 89.5% (17/19) in recurrent AB, and 100% (4/4) in malignant AB, among which the difference is also significant (x2 =7.45, P =0.024).DiscussionAB and OKC are invasive and recurable lesions in jaw, their growth behavior is correlated with multiple factors. PKC is a critical signal molecule involvedin the signal transduction of cell activation and transformation. PKC is relative in oncogenesis, and the role of each isoform is different in individual tumors. The PKC gene is structurally and functionally similar to known oncogenes, some of the isoformes may be namely oncogene. It is presently believed that the interaction between PKC and oncogene, which is dependent on signal pathway, results in malignant transformation of cells.The mechanism by which AB and OKC occur is still not clear, it maybe results from the coeffect of PKC-a with ras and c-myc. PKC isoforms affect the proliferation and differentiation of different cells differently. PKC-a is generally bellieved to contribute to cell differentiation. The fac...
|
PDF Full Text Request