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Expression Significance And Correlation Analysis Of LncRNA MEG3 And E-cadherin In Gastric Cancer

Posted on:2019-11-16Degree:MasterType:Thesis
Country:ChinaCandidate:L L GuanFull Text:PDF
GTID:2404330545954020Subject:Master of Science
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Background and purpose Gastric cancer(GC)is one of the most common malignant tumors in the world.Its morbidity and mortality rate ranked fifth and third among malignant tumors,respectively.According to statistics,there were more than 95 million new cases of global gastric cancer in 2012 and more than 720,000 cases of gastric cancer deaths were located.The number of cases and deaths in China accounts for about half of the world.In spite of the progress in chemotherapy,radiotherapy and surgical techniques for GC in recent years,the survival rate of GC patients remains unsatisfactory.Mainly because GC lacks of early diagnosis,most patients are diagnosed at advanced stage,and there are many difficulties in treatment,recurrence and metastasis monitoring and prognosis evaluation.Although many oncogenes or tumor suppressors have been identified as key players underlying tumorigenesis of GC,however,almost no commonly-accepted biomarkers have been established to facilitate the comprehensive management of patients.Therefore,finding effective GC-specific markers to provide clinical diagnosis and treatment basis for the overall level of GC treatment is of great significance.A growing body of research shows that long non-coding RNA(lnc RNA)plays a crucial regulatory role in various cancers.lnc RNAs may function as oncogenes or tumor suppressors by altering the chromatin structure or by regulating the transcription of protein-coding genes.Maternally expressed gene 3(MEG3)is a tumorsuppressor gene that encodes a noncoding RNA(nc RNA)associated with tumorigenesis.MEG3 is expressed in many normal tissues,while it is frequently either lost,mutated or decreased level in many human tumors and tumor derived cell lines.The study found that MEG3 may be a tumor suppressor gene in gastric cancer.E-cadherin is a calcium-mediated cell adhesion molecule and its abnormal(low)expression has associated with advanced stages and more aggressive behavior of some cancers.Ecadherin is considered to be an inhibitor of tumor metastasis,and its low expression is one of the markers of epithelial-mesenchymal transition(EMT).EMT implies that epigenetic regulation such as histone modification,DNA methylation and micro RNA may be involved.Studies show that some lnc RNAs target E-cadherin to regulate EMT processes.Expression of MEG3 is regulate by epigenetics,MEG3 is abnormal methylation in a variety of tumors.Previous studies in the research group found that the GC cell lines that overexpressed MEG3 obtained the phenotypic characteristics of EMT.How about the mechanism of lnc RNA MEG3 and E-cadherin in GC? Is there a relationship between the two? It's not clear at the moment.In this study,we tested the relative expression of lnc RNA MEG3 and E-cadherin of gastric cancer tissue and the adjacent normal tissue to investigate the correlation between the two markers and detect their relationship with clinical pathological features of patients.Method and Materials 1.Quantitative real-time polymerase chain reaction and immunohistochemistry were used to detect the expression level of lnc RNA MEG3 and E-cadherin in cancer tissues and its paired adjacent normal tissues from 56 GC patients.The correlation of the two markers and their relative expression level with clinical-pathological features were also analyzed.2.The SPSS 21.0 and Graphpad Prism 6.0 were used in this research.It conducted a T-test and ?2-test to find out the salient differences of the expression level of lnc RNA MEG3 and E-cadherin in cancer tissue and its paired adjacent normal tissue;?~2-test was used to analyze whether their expression levels in cancer tissue are related to clinical pathological features respectively.Spearman correlation analysis was used to analyze the correlation of the two markers.Take test significance level ?=0.05,P<0.05 was considered as statistically significant difference.Result 1.Compared with matched normal tissues,the relative expression and positive expression rates of lnc RNA MEG3 and E-cadherin in gastric cancer tissues were significantly reduced(all P<0.05).2.The expression of lnc RNA MEG3 in gastric cancer with lymph node metastasis was significantly lower than that without lymph node metastasis(P=0.033);The larger the tumor,the lower the expression(P=0.038);The later stage,the lower the expression,and the difference was statistically significant(P=0.017);There was no significant correlation between the relative expression level in gastric cancer and gender,age,depth of invasion,pathological type,vascular cancer thrombus,differentiation,distant metastasis and Her-2(P>0.05).3.The expression of E-cadherin in gastric cancer with lymph node metastasis was significantly lower than that without lymph node metastasis(P=0.037);The lower the differentiation,the lower the expression(P=0.038);The larger the tumor,the lower the expression(P=0.008);The later stage,the lower the expression,and the difference was statistically significant(P=0.003);There was no significant correlation between the relative expression level in gastric cancer and gender,age,depth of invasion,pathological type,vascular cancer thrombus,distant metastasis and Her-2(P>0.05).4.The relative expression of lnc RNA MEG3 of cancer tissure has a significantly positive correlation with the relative expression of E-cadherin(P<0.001),and r= 0.651.Conclusions 1.The expression of lnc RNA MEG3 and E-cadherin are low in gastric can-cer.Both of them are related to tumor size,lymph node metastasis,and TNM stage.They may be involved in the occurrence,development and invasion of gastric cancer,and may be used as potential biomarkers to assess the disease.2.The relative expression of lnc RNA MEG3 has a significantly positive correlation with the relative expression of E-cadherin,and the two may have regulatory relationship with each other.
Keywords/Search Tags:LncRNA MEG3, E-cadherin, Gastric cancer, Clinical pathology
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