| Background:Cervical lesions are the most common female lower genital tract lesions, which include cervical intraepithelial neoplasia (cervical intraepithelial neoplasia, CIN) and cervical cancer. Richart first proposed cervical intraepithelial neoplasiain 1997, which includes cervical dysplasia and carcinoma in situ, that is cervical precancerous lesions. The development of cervical lesions to cervical cancer is a long continuous process,the process of so-called precancerous lesions, so early detection and early treatmentto prevent cervical cancer development plays an important role. With the rapid development of molecular biology, it is recognized that the formation and evolution ofcervical cancer is a complex interaction of multiple genes process. Now research on cervical cancer-related genes have more p53, p27, p16, oncogene C-erbβ-2, C-myc, bcl, apoptosis inhibitor survivin, p21, p16 and so on. Currently, the diagnosis ofcervical lesions and treatment rely mainly on pathological results, so the search forbiological markers for diagnosis and treatment as an important indicator of cervical lesions in the process.In recent years, p73 gene is a relatively large number of tumor-related genes. Kaghad of insulin signaling medium connecting zone accidentally discovered p73 gene in 1997. He found that p73 fluorescence in situ hybridization of human malignant tumor located in the hot zone, suggesting that p73 may be the tumor suppressor gene. The structure of the p73 gene transcriptional activation domain, DNA binding, oligomeric functional areas, which is the structure of p53 in a great degree of similarity, it would be classified as a p53 family. However, the structure of the carboxyl terminus of p73 protein and p53 protein structure is different, which makes p73 gene and p53 gene function and difference. This has become a research hotspot in recent years. On p73 in breast cancer, lung cancer, digestive tract cancer research has also been reported.P73 in cervical lesions, but reports are rare. This study was designed on the role of p73 in cervical lesions in a preliminary exploration.P16 protein is reported a novel tumor suppressor gene by Kamb in 1994. It is located on the human chromosome 92P1 area. p16 gene inactivation will lead to uncontrolled cell proliferation. Study confirmed that the tumor suppressor gene promoter region 5'CpG island methylation of the transcriptional level led to an important mechanism for gene inactivation. Now it is been reported in ovarian cancer, esophageal cancer, breast cancer, lung cancer, osteosarcoma, stomach, pancreas, gallbladder, prostate cancer, head and neck malignancy have p16 gene inactivation. a variety of p16 gene in human primary tumors and cell lines mainly homozygous deletion or mutation for the inactivation, which means that lower expression of P16. But in cervical pl6 gene inactivation and expression of p16 is very complex. The reason may be due to high-risk human papilloma virus (HPV) E7 protein expression of protein binding with pRb and leads to inactivation, and inactivation of the Rb gene p16 can stimulate the expression of feedback levels. Salit found that p16 expression was positively correlated with HPVl6/18 the study high-risk HPV and cervical squamous cell carcinoma of the relationship between p16 expression, indicating that p16 overexpression is secondary to the expression of HPV, suggesting that abnormal expression of p16 protein is an early event in tumorigenesis.Currently, the p73, p16's role in the few studies of cervical lesions, cervical lesions both in the relationship and the value of joint detection, there is no relevant reports at home and abroad. Objective:To detect the expression and study the significance of p73 and p16otein in chronic cervicitis,cervical intraepithelial neoplasia(CIN)and cervical cancersamples,and to analyze their correlations.Methods:The S-P immunohistochemical method was used.p73 and p16 protein were detected in one hundred and five cervical specimens, normal cervix(n=18),cervical intraepithelial neoplasia(n=55) and cervical cancer samples(n=32).Results:1) The expression of p73 was found in cell nucleus.The positive ratio of p73 in chronic cervicitis,cervical intraepithelial neoplasia(CIN)and cervical cancer were 92.3%(12/13), 76.4%%(42/55),40.6%(13/32) respectively. The positive expression rate of CIN was significantly lower than that of chronic cervicitis tissues (χ2=10.001, P=0.002. P<0.05), positive expression rate of cervical cancer tissue was significantly lower than CIN, the difference was statistically significant (χ2=11.112, P=0.001. P<0.05).2) The expression of VEGF was found in cytoplasm. The positive ratio of P16 in normal cervical tissue,cervical intraepithelial neoplasia(CIN)and cervical cancer were respectively 15.4%(2/13), 40.0%(23/55), 78.0%(25/32).The positive expression rate of CIN was significantly higher than that of normal cervical tissue, the difference was significant (χ2=15.162, P=0.000. P<0.05); cervical cancer tissues were significantly higher than the CIN group, the difference was statistically significant (χ2 = 6.722, P = 0.01. (P<0.05)).3) The expression of p73 in cervical intraepithelial neoplasia samples was respectively 85.7%(18/21), 72.2%(13/18), 68.8%(11/16).Positive expression rate of the three groups showed no significant (P>0.05). (4) The expression of p16 in cervical intraepithelial neoplasia samples was respectively 14.3%(3/18), 44.4%(8/13), 68.8%(12/16).Comparing the three groups were significantly different (P <0.05). (5) Through the correlation analysis, p73 and p16 in cervical intraepithelial neoplasia and cervical carcinoma correlation r =- 0.901; P = 0.037 (P <0.05).Conclusion:1) The positive expression rate of p73 was decreased graduallyin normal cervical tissue, cervical intraepithelial neoplasia, cervical cancer. The expression of p73 in cervical cancer was significantly lower than normal cervical tissue and cervical intraepithelial neoplasia tissues. Further support may be cervical cancer P73 tumor suppressor gene.2)The positive expression rate of p16 in normal cervical tissue, cervical intraepithelial neoplasia and cervical cancer was increased gradually. The expression of p16 in cervical carcinoma was significantly higher than normal cervical tissues and cervical intraepithelial neoplasia . It is speculated that P16 may be the cervical cancer oncogene.3)p73 and p16 expressionwas negatively correlated in cervical lesions, p16 may play a role in its carcinogenic effect against the tumor suppressor p73, whichinvolved a common occurrence and development of cervical cancer.
|
PDF Full Text Request