Expression And Relativity Research Of P33～(ING1b) And P53 And HPV₁₆ In Cervical Cancer

Tumor suppressor genes is a type of cell growth to control negatively, Loss of its functions caused by gene deletion and/or mutation contributes to cell transformation and tumor formation. INGl, a recently identified candidate tumor suppressor gene, is down regulated than normal tissue. Up to now, the best known and maybe the most important of all tumor suppressor genes is p53 , which is altered in about half of all human tumors, making it the most frequent target for genetic alterations in cancer. In Cervical cancer, inactivation of wild-type p53 is an important molecular event. One reason of p53 gene lost its normal function is gene mutation and produce the type of mutation of P53 protein, another reason is the network related with p53 can not exert regulation as normally. Otherwise, wild-type p53 integrated mutant p53 to lead to p53 gene lost its normal function in cervical cancer, it's an important reason of all reasons. The tumor suppressor gene INGl encoding protein P33^ING1b has a closely relation with wild-type p53 protein, both of them cooperate in regulation of many cell life activities. Therefore, to investigate the cooperating relation of p33(ING1b) and p53 gene in cervical cancer is very significant in theory and practice. Tumor suppressor gene of INGl translates four kinds of proteins of different molecular weight through transcription and shearing way differently, among them, the P33(ING1b) protein is the mainly production of INGl gene Transcript, PSS(ING1b) has a closely relation with P53 protein, both of them cooperate in regulation of many cell life activities. The normal function imperfection or deactivation of pSS(ING1b) may be the important molecule mechanism that the normal cervical tissue malignant conversion. The p33(ING1b) isn't in the signal path upper stream that the signal of p53 mediated, but acting...