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BACKGROUND@#TRIM proteins are important members of E3 ubiquitin ligases, and many studies have confirmed that TRIM family members play an important role in the development of various tumors. We found that TRIM59 expression level in non-small cell lung cancer (NSCLC) was significantly increased through second-generation sequencing. The purpose of this study was to investigate the expression of TRIM59 in NSCLC and its relationship with the clinicopathological parameters as well as the prognosis of patients.@*METHODS@#The Cancer Genome Atlas (TCGA) and Gene Expression Omnibus (GEO) datasets were excavated to analyze the expression of TRIM59 mRNA in NSCLC and its relationship with the prognosis of patients; The expression of TRIM59 protein in 90 tumor tissues and adjacent tissues was detected by immunohistochemical staining, and the relationship between the expression of TRIM59 protein and clinicopathological parameters and prognosis was analyzed.@*RESULTS@#Overexpression of TRIM59 mRNA in tumor tissues predicted poor prognosis. The expression level of TRIM59 protein was significantly higher in tumor tissues than in adjacent tissues, and TRIM59 protein expression was correlated with tumor size (P=0.007), tumor differentiation (P=0.009), tumor-node-metastasis (TNM) stage (P=0.003) and lymph node metastasis (P=0.003). Multivariate Cox regression analyses showed that along with TNM stage, overexpression of TRIM59 could be considered an independent prognostic factor for NSCLC patients.@*CONCLUSIONS@#The expression of TRIM59 is closely related to the prognosis of NSCLC patients, and it is an independent risk factor for NSCLC patients.
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Objective To investigate the expressions of TRIM59,Twist and E-cadherin in hepatocellular carcinoma and their clinical significance. Methods The expressions of TRIM59,Twist and E-cadherin protein were tested by immunohistochemistry in 80 cases of hepatocellular carcinomas and the adjacent paracancerous tissues. Results The positive rate of TRIM59 in hepatocellular carcinoma was significantly higher than that in the adjacent paracancerous tissue(76.3%vs. 8.0%,P<0.05). Significant difference was also observed in the expres-sion rate of Twist between the hepatocellular carcinomas and the paracancerous tissue(66.3%vs. 6.0%,P<0.05). The positive rate of E-cadherin in hepatocellular carcinoma was significantly lower than that in the adjacent para-cancerous tissue(27.5%vs. 90.0%,P<0.05). The differences of the expression of TRIM59 in hepatocellular carci-noma of pathological grading,tumor differentiation,vascular invasion and clinical TNM stage were significant(P<0.05). The differences of the expression of Twist in hepatocellular carcinoma of pathological grading ,differentia-tion,vascular invasion and clinical TNM stage was also significant(P<0.05,respectively). The differences of the expression of E-cadherin in hepatocellular carcinoma of pathological grading,differentiation,vascular invasion and clinical TNM stage were also significant(P<0.05,respectively). Significantly positive correlation was also found between TRIM59 and Twist by using spearman correlation analysis(P<0.05). Negative correlations were observed between TRIM59 and E-cadherin(P < 0.05),and between Twist and E-cadherin(P < 0.05). Survival analysis showed that TRIM59 expression was an independent prognostic factor in hepatocellular carcinoma. Conclusion TRIM59,Twist and E-cadherin protein expression might be associated with the development,invasion,and metas-tasis of hepatocellular carcinoma. TRIM59 may become a new target gene for the treatment of human hepatocellular carcinoma.
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Objective · To demonstrate the effect of TRIM59 on gliomagenesis and the molecular mechanism.Methods · TRIM59 protein expression in glioma specimens was analyzed by immunohistochemical staining,and in several glioma cell lines by Western blotting and quantative PCR.After TRIM59 was knocked down by shRNAs,cell proliferation,migration,colony formation,and orthotopic xenograft brain tumor development were detected.The signaling pathway of TRIM59 in gliomas was also explored by RNA-Seq and KEGG PATHWAY analyses.Results· The levels of TRIM59 protein expression in clinical glioma specimens were positively correlated with glioma malignancy.TRIM59 was highly expressed in LN229 and U87 glioma cells compared with normal human astrocytes.Knockdown of TRIM59 in these two cell lines with lentivirus-mediated shRNAs inhibited their proliferation,migration,and colony formation.Compared with the control xenograft models,knockdown of TRIM59 significantly inhibited glioma tumor growth.RNASeq and KEGG PATHWAY analyses identified that TRIM59 knockdown down-regulated 306 genes,among which PI3K/AKT signal pathway-related genes were the most.Moreover,TRIM59 knockdown suppressed AKT phosphorylation,whereas overexpression of a constitutively actived AKT (Myr-AKT)rescued TRIM59 knockdown-inhibited cell proliferation.Conclusion· TRIM59 is a new glioma oncogene,which may take effect through activating PI3K/AKT signaling pathway.