PTBP1 is a Novel Poor Prognostic Factor for Glioma.

Objective: Polypyrimidine tract-binding protein 1 (PTBP1) is an RNA-binding protein, which plays a role in pre-mRNA splicing and in the regulation of alternative splicing events. However, little was known about the correlation between PTBP1 and glioma and its prognostic significance in glioma patients. Our aim was to investigate the expression, functional role, and prognostic value of PTBP1 in glioma. Methods: We explored the expression of PTBP1 protein using immunohistochemistry in 150 adult malignant glioma tissues and 20 normal brain tissues and evaluated its association with clinicopathological parameters by chi-square test. Kaplan-Meier method was used to evaluate the prognostic effect of PTBP1 in glioma. Univariate/multivariate Cox analyses were used to identify independent prognostic factors. Transcriptional regulation network was constructed based on differentially expressed genes (DEGs) of PTBP1 from TCGA/CGGA database. GO and KEGG enrichment analyses were used to explore the function and pathways of DEGs. Results: Out of the 150 malignant glioma tissues (60 LGG and 90 GBMs) and 20 normal brain tissues in our cohort, PTBP1 protein was high expressed in glioma tissues (79/150, 52.7%), but no expression was detected in normal brain tissues (0/20, 0%). The expression of PTBP1 was significantly higher in GBMs (P < 0.001). More than half of GBMs (62/90, 68.9%) were PTBP1 high expression. Chi-square test showed that the expression of PTBP1 was correlated with patient age, WHO grade, Ki-67 index, and IDH status. High expression of PTBP1 was significantly associated with poor prognosis in glioma, and it was an independent risk factor in glioma patients. Furthermore, we shed light on the underlying mechanism of PTBP1 by constructing a miR-218-TCF3-PTBP1 transcriptional network in glioma. Conclusion: PTBP1 was high expressed in glioma, and it significantly correlated with poor prognosis, suggesting a potential therapeutic target for glioma, particularly for GBM.

EMX2OS plays a prognosis-associated enhancer RNA role in gastric cancer.

ABSTRACT: Enhancer RNAs (eRNAs), a subclass of lncRNAs, are derived from enhancer regions. The function of eRNAs has been reported by many previous studies. However, the role of eRNAs in gastric cancer, especially the prognosis-associated eRNAs, has not been studied yet.In this study, we have used a novel approach to screened key eRNAs in gastric cancer. Kaplan-Meier correlation analysis and Co-expression analysis were used to find the most significant survival-associated eRNAs. Enrichment analysis is applied to explore the key functions and pathways of screened eRNAs. The correlation and survival analysis are used to evaluate targeted genes in the pan-cancer analysisA total of 63 prognostic-associated eRNAs in gastric cancer were identified, the top 6 eRNAs were LINC01714, ZNF192P1, AC079760.2, LINC01645, EMX2OS, and AC114489.2. The correlation analysis demonstrated the top 10 screened eRNAs and their targeted genes. The results demonstrated that EMX2OS was ranked as the top eRNA according to the results of the Kaplan-Meier analysis. The correlation analysis demonstrated that eRNA EMX2OS is correlated with age, grade, stage, and cancer status. The pan-cancer analysis demonstrated that EMX2OS was associated with poor survival outcomes in adrenocortical carcinoma, cervical squamous cell carcinoma and endocervical adenocarcinoma, kidney renal clear cell carcinoma, stomach adenocarcinoma, and uveal melanoma.In this study, survival-related eRNAs were screened and the correlation between survival-related eRNAs and their targeted genes was demonstrated. EMX2OS plays a prognosis-associated eRNA role in gastric cancer, which might be a novel therapeutic target in clinical practice.

[Effects of salvianolic acid B on cardiovascular endothelial cells and platelet activation in a rabbit model of ischemia-reperfusion].

OBJECTIVE: To investigate the effects of salvianolic acid B (SA-B) on cardiovascular endothelial cell function and platelet activation during myocardial ischemia-reperfusion in rabbits. METHODS: A total of 24 New Zealand white rabbits were randomly divided into sham-operated group, ischemia-reperfusion group (untreated group) and SA-B group. The hearts of rabbits in untreated group and SA-B group underwent half an hour of left anterior descending coronary artery (LADCA) occlusion via ligation technology, which was followed by 4 hours of reperfusion to prepared ischemia-reperfusion injury model in vivo. For sham-operated group, the animals were not subjected to occlusion of LADCA. In SA-B treatment group the rabbits were intravenously administered SA-B immediately after LADCA occlusion, and the other two groups were given normal saline in the same way instead of SA-B. The jugular vein bloods of animals were collected before LADCA ligation, half an hour after ligation and after 1-, 4-hour reperfusion, respectively. The content of plasma nitric oxide (NO) was determined by nitrate reductase process. Radioimmunoassay was applied to detect the endothelin (ET) content in plasma and the count of alpha-granule membrane protein-140 (GMP-140) on platelet surface to identify the activation of the platelet. RESULTS: No significant difference was observed before and after sham LADCA occlusion in sham-operated group in the contents of NO and ET in plasma (P>0.05), neither was the count of GMP-140 on platelet surface (P>0.05). The content of NO in plasma detected 0.5 h after LADCA occlusion was significantly decreased in untreated group compared with the sham-operated group at the corresponding time, and they were also much lower than that before LADCA occlusion in the sham-operated group (P<0.05). The plasma content of NO in untreated group showed a progressive decrease in response to the myocardial reperfusion. However, the content of ET in plasma and the count of GMP-140 on platelet surface were remarkably increased after myocardial ischemia as compared with those before LADCA ligation and those detected in sham-operated group (P<0.05). The content of ET and the count of GMP-140 in the untreated group were further increased corresponding to the aggressive reperfusion. The content of NO was significantly increased while the content of ET and the count of GMP-140 were both significantly decreased in SA-B group as compared with untreated group after 1- and 4-hour myocardial reperfusion, respectively (P<0.01). CONCLUSION: The results show that endothelial dysfunction and platelet activation occur during ischemia-reperfusion in rabbit hearts in vivo and SA-B protects cardiovascular endothelium cells against ischemia-reperfusion injury and inhibits the activation of platelet during myocardial ischemia and reperfusion.