Long noncoding RNAs cancer susceptibility candidate 2 (CASC2) have been demonstrated as playing crucial regulatory roles in a few of cancers. However, the biological function of lncRNA CASC2 in bladder cancer are still unclear. In this study, we found that lncRNA CASC2 was significantly down-regulated in bladder cancer tissues and cell lines by quantitative real time-PCR and associated with advanced TNM stage (III/IV). Moreover, overexpression of lncRNA CASC2 remarkably reduced the cell growth, migration and invasion, as well as promoted early apoptosis of bladder cancer cell in vitro. Furthermore, we illustrated that lncRNA CASC2 inhibited Wnt/β-catenin signal pathway activity by decrasing the β-catenin expression and reversing the downstream target gene expression of Wnt signaling pathway. Taken together, lncRNA CASC2 plays an pivotal role in bladder tumorigenesis and progression and may act as a potential biomarker for the treatment of bladder cancer.

The purpose of the present study was to explore the role and mechanism of extracellular ecto-5'-nucleotidase (CD73) in human colorectal cancer growth. Firstly, CD73 expression was detected in colorectal cancer cell lines both at the mRNA and protein levels. Secondly, recombinant CD73 interference and overexpression lentiviruses were used, respectively. Colony formation assay, CCK-8 assay and flow cytometry were used to investigate the impact of CD73 on colorectal cancer cell proliferation and cell cycle distribution. Then, adenosine and CD73 enzyme activity inhibitor (APCP) were used to study the effect of CD73 on Epidermal growth factor receptor (EGFR) and β-catenin/cyclin D1 signaling pathways. Finally, a human colorectal cancer transplantation nude mouse model was used to observe the effect of CD73 on tumor growth in vivo. As the results showed, CD73 was highly expressed in the colorectal cancer cell lines. CD73 promoted colorectal cancer cell proliferation both in vivo and in vitro. CD73 activated EGFR and the β-catenin/cyclin D1 signaling pathways through its enzyme and non-enzyme activities. All of the results confirmed that CD73 promotes the growth of human colorectal cancer cells through EGFR and the β-catenin/cyclin D1 signaling pathway. CD73 may be used as a valuable biomarker of colorectal cancer.

Background: To investigate the expression of methyltransferase 3 (METTL3) and its relationship with 18 F-FDG uptake in patients with esophageal carcinoma (ESCA). Materials and methods:This study analyzed the expression of METTL3 in ESCA and its relationship with clinicopathological features by The Cancer Genome Atlas (TCGA) database. Immunohistochemical staining was performed on 57 tumor tissues of ESCA patients who underwent PET/CT scan before surgery to evaluate the expression of METTL3, glucose transporter 1 (GLUT1), and hexokinase 2 (HK2) in tumor tissues and peritumoral tissues. Analyze the relationship between SUVmax with METTL3, HK2, and GLUT1 expression. Results: The expression of METTL3, GLUT1, and HK2 was significantly increased in ESCA tissues compared with normal tissues (p < 0.001). The expression of METTL3 was correlated with tumor size and histological differentiation (p < 0.05), and there was no significant difference between age, sex, pathological types, tumor staging, or lymph node metastasis (p > 0.05). The SUVmax was significantly higher in tumors with high METTL3 expression (17.822±6.249) compared to low METTL3 expression (9.573±5.082) (p < 0.001). There was a positive correlation between the SUVmax and METTL3 expression in ESCA (r 2 = 0.647, p < 0.001). Multivariate analysis confirmed the association between SUVmax and METTL3 expression (p < 0.05). GLUT1 and HK2 expression in ESCA was positively correlated with 18 F-FDG uptake and METTL3 status (p < 0.001). Conclusions: The high expression of METTL3 is related to the high SUVmax in ESCA, and METTL3 may increase 18 F-FDG uptake by regulating GLUT1 and HK2.

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BackgroundOverexpression of NPM1 can promote the growth and proliferation of various tumor cells. However, there are few studies on the comprehensive analysis of NPM1 in lung adenocarcinoma (LUAD).MethodsTCGA and GEO data sets were used to analyze the expression of NPM1 in LUAD and clinicopathological analysis. The GO/KEGG enrichment analysis of NPM1 co-expression and gene set enrichment analysis (GSEA) were performed using R software package. The relationship between NPM1 expression and LUAD immune infiltration was analyzed using TIMER, GEPIA database and TCGA data sets, and the relationship between NPM1 expression level and LUAD m6A modification and glycolysis was analyzed using TCGA and GEO data sets.ResultsNPM1 was overexpressed in a variety of tumors including LUAD, and the ROC curve showed that NPM1 had a certain accuracy in predicting the outcome of tumors and normal samples. The expression level of NPM1 in LUAD is significantly related to tumor stage and prognosis. The GO/KEGG enrichment analysis indicated that NPM1 was closely related to translational initiation, ribosome, structural constituent of ribosome, ribosome, Parkinson disease, and RNA transport. GSEA showed that the main enrichment pathway of NPM1-related differential genes was mainly related to mTORC1 mediated signaling, p53 hypoxia pathway, signaling by EGFR in cancer, antigen activates B cell receptor BCR leading to generation of second messengers, aerobic glycolysis and methylation pathways. The analysis of TIMER, GEPIA database and TCGA data sets showed that the expression level of NPM1 was negatively correlated with B cells and NK cells. The TCGA and GEO data sets analysis indicated that the NPM1 expression was significantly correlated with one m6A modifier related gene (YTHDF2) and five glycolysis related genes (ENO1, HK2, LDHA, LDHB and SLC2A1).ConclusionNPM1 is a prognostic biomarker involved in immune infiltration of LUAD and associated with m6A modification and glycolysis. NPM1 can be used as an effective target for diagnosis and treatment of LUAD.

Long noncoding RNA (lncRNA) colon cancer-associated transcript 2 (CCAT2) has been demonstrated to play an important role in diverse tumorigenesis. However, the biological function of lncRNAs in glioma is still unknown. In this study, we found that lncRNA CCAT2 was overexpressed in glioma tissues and cell lines and associated with tumor grade and size. Furthermore, patients with high levels of lncRNA CCAT2 had poorer survival than those with lower levels of lncRNA CCAT2. Knocking down lncRNA CCAT2 expression significantly suppressed the glioma cell growth, migration, and invasion, as well as induced early apoptosis of glioma cells in vitro. Moreover, lncRNA CCAT2 regulated epithelial-mesenchymal transition (EMT)-associated gene expression. In conclusion, lncRNA CCAT2 plays an important role in glioma tumorigenesis and progression and may act as a potential biomarker for therapeutic strategy and prognostic prediction.

BackgroundGlucose transporter 1 (GLUT1) is encoded by the solute carrier family 2A1 (SLC2A1) gene and is one of the glucose transporters with the greatest affinity for glucose. Abnormal expression of GLUT1 is associated with a variety of cancers. However, the biological role of GLUT1 in esophageal carcinoma (ESCA) remains to be determined.MethodsWe analyzed the expression of GLUT1 in pan-cancer and ESCA as well as clinicopathological analysis through multiple databases. Use R and STRING to perform GO/KEGG function enrichment and PPI analysis for GLUT1 co-expression. TIMER and CIBERSORT were used to analyze the relationship between GLUT1 expression and immune infiltration in ESCA. The TCGA ESCA cohort was used to analyze the relationship between GLUT1 expression and m6A modification in ESCA, and to construct a regulatory network in line with the ceRNA hypothesis.ResultsGLUT1 is highly expressed in a variety of tumors including ESCA, and is closely related to histological types and histological grade. GO/KEGG functional enrichment analysis revealed that GLUT1 is closely related to structural constituent of cytoskeleton, intermediate filament binding, cell-cell adheres junction, epidermis development, and P53 signaling pathway. PPI shows that GLUT1 is closely related to TP53, GIPC1 and INS, and these three proteins all play an important role in tumor proliferation. CIBERSORT analysis showed that GLUT1 expression is related to the infiltration of multiple immune cells. When GLUT1 is highly expressed, the number of memory B cells decreases. ESCA cohort analysis found that GLUT1 expression was related to 7 m6A modifier genes. Six possible crRNA networks in ESCA were constructed by correlation analysis, and all these ceRNA networks contained GLUT1.ConclusionGLUT1 can be used as a biomarker for the diagnosis and treatment of ESCA, and is related to tumor immune infiltration, m6A modification and ceRNA network.

Here, we used a noninvasive multimodality imaging approach to monitor differentiation of transplanted bone marrow mesenchymal stem cells (BMSCs) and recovery of cardiac function in an in vivo model of myocardial infarction (MI). We established a rat MI model by coronary artery ligation. Ninety rats were randomly assigned into four groups: sham-operated, MI model, and α-MHC-HSV1-tk-transfected or un-transfected BMSCs-treated MI model. We used 18F-Fluro-deoxyglucose (18F-FDG) positron emission tomography (PET) to monitor recovery of cardiac function, and 18F-FHBG PET/CT imaging to monitor transplanted BMSCs differentiation 24 h after 18F-FDG imaging. The uptake of 18F-FDG at 3, 16, 30 and 45 days after BMSCs injection was 0.39 ± 0.03, 0.57 ± 0.05, 0.59 ± 0.04, and 0.71 ± 0.05% ID/g, respectively. Uptake of 18F-FHBG increased significantly in large areas in the BMSCs-treated group over time. Ex vivo experiments indicated that expression of the cardiomyocyte markers GATA-4 and cardiac troponin I markedly increased in the BMSCs-treated group. Additionally, immunohistochemistry revealed that HSV-tk-labelled BMSCs-derived cells were positive for cardiac troponin I. Multimodal imaging systems combining an α-MHC-HSV1-tk/18F-FHBG reporter gene and 18F-FDG metabolism imaging could be used to track differentiation of transplanted BMSCs and recovery of cardiac function in MI.