Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:4.1.1.6 (CAD)
 4,420 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Background: The MALAT1, MIAT, and XIST long noncoding RNAs (lncRNAs) participate in the pathogenesis of complex diseases and also serve as diagnostic markers. The study aimed to assess their expressions in CAD patients with or without T2DM against diabetic and non-diabetic controls.Methods: The expression levels of three lncRNAs in 50 CAD patients (with or without diabetes) and 50 non-CAD subjects (with or without diabetes) were evaluated by using the TaqMan Assay method.Results: MALAT1 and MIAT were upregulated in CAD patients (p Value= .0008 and .0078, respectively). The expression level of XIST was significantly elevated diabetic compared to non-diabetic CAD patients (p Value= .0003). MALAT1 gene had the highest diagnostic power for discrimination of CAD patients from controls (AUC= 0.682, p Value=.001).Conclusions: The current study supports the participation of lncRNAs in the pathogenesis of CAD and T2DM and highlights their potential as diagnostic biomarkers.
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PMID:Variation in the expression level of MALAT1, MIAT and XIST lncRNAs in coronary artery disease patients with and without type 2 diabetes mellitus. 3244 81

The tumor resistance of glioblastoma cells in vivo is thought to be enhanced by their heterogeneity and plasticity, which are extremely difficult to curb in vitro. The external microenvironment shapes the molecular profile of tumor culture models, thus influencing potential therapy response. Our study examines the expression profile of selected lncRNAs involved in tumor resistance network in three different glioblastoma-derived models commonly utilized for testing drug response in vitro. Differential expression analysis revealed significant divergence in lncRNA profile between parental tumors and tumor-derived cell cultures in vitro, including the following particles: MALAT1, CASC2, H19, TUSC7, XIST, RP11-838N2.4, DLX6-AS1, GLIDR, MIR210HG, SOX2-OT. The examined lncRNAs influence the phenomenon of tumor resistance via their downstream target genes through a variety of processes: multi-drug resistance, epithelial-mesenchymal transition, autophagy, cell proliferation and viability, and DNA repair. A comparison of in vivo and in vitro expression identified differences in the levels of potential lncRNA targets, with the highest discrepancies detected for the MDR1, LRP1, BCRP and MRP1 genes. Co-expression analyses confirmed the following interrelations: MALAT1-TYMS, MALAT1-MRP5, H19-ZEB1, CASC2-VIM, CASC2-N-CAD; they additionally suggest the possibility of MALAT1-BCRP, MALAT1-mTOR and TUSC7-PTEN interconnections in glioblastoma. Although our results clearly demonstrate that the artificial ex vivo microenvironment changes the profile of lncRNAs related to tumor resistance, it is difficult to anticipate the final phenotypic effect, since this phenomenon is a complex one that involves a network of molecular interactions underlying a variety of cellular processes.
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PMID:If Artificial In Vitro Microenvironment Can Influence Tumor Drug Resistance Network via Modulation of lncRNA Expression?-Comparative Analysis of Glioblastoma-Derived Cell Culture Models and Initial Tumors In Vivo. 3324 8