| The relation between apoptosis and tumor absorbed more eyes these years. It was believed that multicellular organism maintained their stability by cell proliferation and apoptosis, and tumor would occur once the balance was broken. Even through evidences showed that many tumor cells could resist apoptosis, the mechanism was still a mystery. Nuclear transcription factor κB (NF-κB) was firstly found by Ranjan Sen etc. in the B lymphocyte in 1986, which was one of the most important transcription factors and named from the special binding with the enhancer κB sequence of immunoglobulin kappa light chain gene. Comprehensive study on NF-κB was made by many researchers, and articles relating to NF-κB were often found in famous journals such as Science, Nature, Cell and so on. Recent founding showed that NF-κB played a key role in tumor anti-apoptosis mechanism. As we all know, the biological features of tumor cell were abnormal proliferation and immortalization, which usually expressed as apoptosis deficiency. The activation of NF-κB was the primary mechanism of tumor cell resisting the apoptosis mediated by tumor necrosis factor (TNF). New research showed that NF-κB had a close connection with the occurrence and develop of few human malignant tumors including oral squamous cell carcinoma (SCC).The study would establish the animal models of malignant transformation in hamster buccal mucosa by DMBA (0.5%), examine the expression and significance of p65——an important subunit of nuclear transcription factor κB (NF-κB) and its inhibitory protein IκBα in malignant transformation of hamster buccal mucosa., and discuss the mechanism of p65 processing in the malignant transformation of hamster buccal mucosa and early diagnosis and gene therapy of oral carcinoma.So far it was proved that there were 5 NF-κB family members in the mammalian cells, in which p65(RelA)was an important subunit, and the heterodimers formatted by p65 and p50 was the most common pattern. The N ends of this family members had a very conservative Rel-homology domain(RHD)combined by about 300 amino acid residues, including DNA recognition sequence and nuclear localization signal (NLS). The NF-κB heterodimers and its inhibitory protein IκBα formatted as complex in the cytoplasmic plasm when resting. By non-covalence combination, IκB hided the nucleic localization signal of NF-κB to prevent the nucleic dislocation of NF-κB. Once activated by the signal molecule, IκBα degraded after being phosphorylated, and NF-κB was released from IκBα, activated, translocated into the nuclear, and connected with DNA NF-κB component to induce the gene transcription which relied on.IκB was one kind of inhibitory protein of NF-κB. IκBα was a member of IκB family found earlist and studied most clear. The relative molecular weight of it was 3.7KD, and IκBα was combined with 3 parts in construction including: the base of controlling the activation of NF-κB, i.e. the N end structure domain which could start phosphorylation under the stimulation of signal; the connection part with NF-κB, i.e. 5 ankyrin repeated sequences; the C end, i.e. a tetra-peptide structure domain which took part in the basic transition of protein. IκBα itself was a react gene of NF-κB, and in the controlling domain located in the upper stream of gene promoter there was a κB site. Hence the activation of NF-κB could up-regulate IκBα, then inhibited the activating process of NF-κB by such a feedback manner to prevent the super-activation of it.To discuss the expression of p65 in the carcinomatous process of oral mucosa epithelia, we established the animal models of malignant transformation in hamster buccal mucosa by DMBA (0.5%), and verified the results of animal experiment with histophthology manner. The expression of p65and IκBα in the process covering normal buccal mucosa, epithelial hyperplasia, epithelial dysplasia and squamous cell carcinoma (SCC) were systemically examined. Western blot found that in normal buccal epit...
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