Tropomyosin3 Is Associated With Invasion, Migration And Prognosisin Esophageal Squamous Cell Carcinoma

Background:Esophageal carcinoma is one of leading causes of death in the world. Esophageal cancer with esophageal adenocarcinoma isprominent in the European and American countries, but the region are mainly composed of esophageal squamous cell carcinomasin our country,and 5 years of survival rate of esophageal cancer in China is poorly around 25-40%with prognosis.The main reason is that esophageal cancer early diagnosis is difficult to diagnose, once found basically is given priority to with middle-late, which most of them are lose the chance of radical surgery. Targeted therapy is currently unclear in esophageal cancer.Therefore, seeking for esophageal cancer specific molecular markers to guide the early diagnosis, biological target therapy is particularly important.The occurrence of esophageal cancer is a complicated process, involving many stage, multiple genes and multiple factors. Therefore, the complex pathogenesis is difficult to overcome an important cause of esophageal cancer. Although the molecular markers have been founded a lot of exciting results in esophageal cancer, yet has not a useful marker in clinical practice.This article research was mainly carried out early proteomics differences in screening protein, using cytology experiment to verify the differences between the biological function of protein. Toseek for differences in protein molecular markers provide theory basis for esophageal cancer of biological targets, andimprove the treatment of early esophageal cancer diagnosis and prognosis. Material and methods:We selected EC109 and EC9706 esophageal cancer cell lines as experimental, through a small interfering RNA(RNAi) technology knockout tropomyosin3(TPM3).These cells are in the best state for transfection TPM3 small interference RNA(TPM3-oligo).Groped through experimental conditions knockout TPM3 optimum conditions were determined in a series of experiments including, wounding healing assay, cell migration and invasion assay, plate cloning experiment, cell proliferation, protein and TPM3 related mechanism research.Collectedthe Union Clinical Medical College of Fujian Medical University in 2005-2009 specimens of esophageal cancer, including cancer and cancer adjacent tissues, immunohistochemical through TPM3 dyeing experiments, using statistical carcinoma tissue and immune omics grading method by TPM3 expression, using SPSS 19.0 software for Kaplan Meier methods to analyze.Results:TPM3 cells significantly inhibited the ability of migration and invasion after the silence of TPM3.At the same time, we found inhibition of clone formationafter konckdown TPM3.Beside, in the carcinoma and clinical specimens, we found TPM3 were 53.11% of cancer tissue was obviously higher than that of 7.34% of the tissue adjacent to carcinoma(P < 0.05).And we find that with high expression of TPM3 in cancers patients with the poor prognosis(the Log Rank, P = 0.015).Concluding:In histology, we found that the high expression of TPM3 related to the prognosis of esophageal cancer. We find that with high expression of TPM3 in cancers patients with the poor prognosis. TPM3 protein silence can obviously inhibit the migration and invasion of esophageal cancer.