The Expression Of Plk1 And Survivin In Esophageal Squamous Cell Carcinoma

Background and objectiveEsophageal carcinoma is one of the common malignant tumors which is threatening human health. More than 95 percent Esophageal cancer are squamous cell cancer. At present, the etiology and pathogenesis of esophageal carcinoma is still unclear. Presumably as other solid tumors, its occurrence, development and invasion, transference should be a multi-factor and multi-step process, involving mechanisms of disorders of cancer-suppressor genes and oncogenes in expression, cell cycle and apoptosis regulations anomalies etc.The number and quality of cells determines the formation of human organ structures and the execution of function, cells increase the number by mitosis, participating in embryonic formation and shaping it through apoptosis.Cell proliferation and apoptosis are in a dynamic balance,which is of important significance for the embryonic development and regulation of the body steady state. Throughout the cell cycle, cell proliferation and apoptosis are regulated by a strict and precise means, dysfunction of any part of regulations could lead to unlimited cell proliferation and apoptosis inhibition to induce tumor formation. Thus, cell cycle-related kinases regulating of cell proliferation and enzymes mediating apoptosis play an important role in the process of cancer formation.Plkl is a highly conservative serine/threonine kinase that plays an important role in mammalian cell mitosis. Researches show that Plkl has an abnormal increase in a variety of malignant tumors while regarding as an independent prognosis factor. Survivin is a new member of apoptosis protein inhibitor factor family, which is so far the strongest apoptosis inhibitor factor, also high expression in many malignancies. Survivin is a downstream molecule of Plkl, both of them participate in formation of esophageal squamous cell carcinomas by means of interfering with the cell cycle, inhibiting cell apoptosis, regulating tumor angiogenesis.This study using RT-PCR researches the expression of Plkl and Survivin in esophageal squamous cell carcinoma, while trying to explore the mechanisms in process of forming of esophageal squamous cell carcinoma and the relationship with common clinical and pathological features of esophageal squamous cell carcinoma, so as to further provide theoretical basis for the gene diagnosis and gene therapy of esophageal squamous cell carcinoma.Materials and methods1. As experimental group,fifty cases were obtained from the patients with esophageal squamous cell carcinoma who underwent resection in our hospital from October 2009 to June 2010.Among them,28 males and 22 females, age range 43-81,average age 58.8. Fifty cases of normal esophageal tissue are selected as control groups, which were obtained from the patients with esophageal squamous cell carcinoma and 5cm far from cancer tissues. All cases with complete clinical data and pathologic diagnosis have never been applied with chemotherapy and radiotherapy before operation.2. RT-PCR is employed to determinate the gene expression of Plkl and Survivin in the 50 cancer tissues and 50 normal tissues adjacent to cancer,while analysing the relationship of gene expression of Plkl,Survivin and clinical pathological feature in cancer tissues.3.SPSS13.0 is used for all analysis,including two groups of independent sample comparison design using t test, multiple groups using single factor analysis of variance and obtainment of the connection between the two indexes using Pearson correlation analysis,a=0.05.Result 1. The expression of PlklmRNA in esophageal squamous cell carcinoma tissues is significantly higher than normal tissues adjacent to cancer (2.103±0.206 vs 0.195±0.017, p<0.05).2. The expression of Survivin mRNA in esophageal squamous cell carcinoma tissues is significantly higher than normal tissues adjacent to cancer (1.852±0.230 vs 0.132±0.026, p<0.05).3. There is no obvious difference in expression of PlklmRNA,SurvivinmRNA between different gender, age in esophageal squamous cell carcinoma tissues (p> 0.05)4.The mean expression of PlklmRNA in the group that belonging to esophageal fiber membrane invaded is significantly higher than that in controls (2.013±0.200,2.201±0.262 p<0.05). The expression of PlklmRNA is obviously different between lymph node metastasis group and the control one (2.143+0.187 1.884+0.286 p< 0.05). There is a significant difference between high-moderately differentiated group and low-undifferentiated one (2.031+0.2442.210+0.178 p< 0.05). The expressions of PlklmRNA in different TNM esophageal squamous cell carcinomas tissue are respectively:Ⅰ1.697+0.044,Ⅱ2.066+0.337,Ⅲ2.134 +0.154 (p<0.05).5. The mean expression of Survivin mRNA in the group that belonging to esophageal fiber membrane invaded is significantly higher than that in controls (1.780±0.196,1.979±0.236 p<0.05). The expression of Survivin mRNA is obviously different between lymph node metastasis group and the control one (1.896±0.189,1.710±0.296 p< 0.05). There is a significant difference between high moderately differentiated group and low-undifferentiated one (1.802±0.241,1.981±0.136 p< 0.05). The expressions of Survivin mRNA in different TNM esophageal squamous cell carcinomas tissue are respectively: I 1.482+0.042,Ⅰ1.880±0.161,Ⅲ1.894±0.312 (p< 0.05).6. Pearson correlation analysis showed that the expression of PlklmRNA and Survivin mRNA in esophagus squamous cell carcinoma is positively correlated (r=0.549,p<0.05)Conclusion 1. There is a certain relevance between the occurrence and development of esophageal squamous cell carcinoma and excessive expression of Plk1 and Survivin.2. Plk1 and Survivin are tend to overexpression in process of the occurrence and development of esophageal squamous cell carcinoma.Both are positively correlated and synergistic.3.Overexpression of Plk1 and Survivin in esophageal squamous cell carcinoma is irrelevant with gender and age of the patients,closely correlated with whether invasion of esophageal fiber membrane by tumor, whether distant lymph node metastasis, differentiation degree of tumor and TNM stage.