The Expression Of P33ING1 In Oral Premalignant Iesions And Squamous Cell Carcinomas

Background: Molecule mechanism of tumour invasion is revealled gradually and the molecular biology techniques has development day by day ,so oncogene , anti-oncogene and the therapeutics to aim directly at oncogene and anti-oncogene has become a hot spot .The alteration of cancer-related genes will induce the occurrence of carcinoma ,and the inactivation or loss of anti-oncogene plays an important role in the development of the carcinoma. As a new and important tumor suppressor gene,ING1 has caused people increasingly widespread concern, since 1996 when Garkavtsev deploy substractive hybridization to clone it.The present results show ING1 can inhibite cell growth, regulate cell senescence and induce apoptosis.As the"molecule partner"of p53, p33ING1 can cooperation with p53 in the process of cell cycle regulation. In addition, it also participate the regulating transcription as a transcription factor.Many tumors have been found to have abnormal expression of p33ING1.Studies on primary gastric cancer,hematological system tumor,breast cancer,neuroglioma and squamous cell carcinoma of head and neck have shown that the lowexpression of p33ING1 closely relates with the occurrence and development of those tumor and the olig-expression includes gene mutation,rearrangement ,deletion and loss of expression and other ways to reduce the level of expression.Oral squmous cell carcinoma (OSCC) is one of the most commom oral cancers,which is a serious threat to human health with a very high morbidity and a low survival rate.The transmutation of structure and function of oncogene and anti-oncogene influences the development of OSCC. We study the expression of p33ING1 in oral premalignant lesions and squamous cell carcinomas.Objective: To detect the expression of p33ING1 in OSCC and to explore its role in the development of OSCC and its future prospects.Methods: From August 2005 to November 2006, we obtained 75 samples from the stomatology hospital of Jilin university , including 8 cases of normal oral mucous,7 cases of hyperplasia epithelia,30 cases of dysplasis epithelia and 30 cases of oral squamous cell carcinoma(OSCC).We detected the expression of p33ING1 protein and ing1 mRNA by immunohistochemistry andreverse transcriptase-polymerase chain reaction (RT-PCR), respectively.Results:1.The positive expression of p33ING1 protein in normal oral mucous group, epithelia hyperplasia group, epithelia dysplasis group and OSCC was 100%,100%,83.3% and 60%.There were no significant difference in p33ING1 expression between oral mucous group and epithelia hyperplasia group and between epithelia hyperplasia group and epithelia dysplasis group(P>0.05). There were significant difference between OSCC and any other group(P<0.05).2. The positive expression rate of p33ING1 protein in 13 male and 17 female were 53.8% and 64.7%.There were no significant difference between them. The positive expression rate of p33ING1 protein in 12 cases of lymph node metastasis and 18 cases without lymph node metastasis were 33.3% and 77.8%. There were significant difference between them. The positive expression rate of p33ING1 protein in high ,medium,and low expression were 33.3%,82.2%and 60%. There were no significant difference between any two of them.3.We detected the expression of ing1 mRNA in all oral mucoustissue and epithelia hyperplasia tissue . We detected the expression of ing1 mRNA in 25 epithelia dysplasis tissue and 25 OSCC . There were significant difference between normal oral mucous group, epithelia hyperplasia group and epithelia dysplasis group , OSCC .Except that there were no significant difference in ing1 mRNA expression between oral mucous group and epithelia hyperplasia group (P>0.01),there were significant difference between any two group.Conclusion:1. Immunohistochemistry results show that the positive rate of p33ING1 protein in the cancers tissues were significantly lower than those in normal issues and epithelia dysplasis group .2. RT-PCR results show that the expression level of ing1 mRNA in the cancerous tissues were significantly lower than those in normal tissues and epithelia dysplasis group by RT-PCR.3.The expression of p33ING1 protein in the cancerous tissues has no manifest dependability wit sex and age.The expression of p33ING1 protein degraded in poor differentiation OSCC. The positive rate of p33ING1 protein expression degraded conspicuouslyin the OSCC without lymphatica diversion.4.The expression level of p33ING1 is down regulation or absence from normal tissues , epithelia dysplasis tissues to OSCC .It reveals that the gene mutation or deletion may play an important role on the development of OSCC.