Long noncoding RNAs (lncRNAs) have emerged as key regulatory molecules at almost every level of gene expression regulation. The altered expression of lncRNAs is a characteristic of numerous types of cancer, and lncRNAs have been demonstrated to promote the development, invasion and metastasis of tumors through various mechanisms. However, the role of lncRNAs in papillary thyroid carcinoma (PTC) remain unclear. In the present study, differentially expressed lncRNAs and mRNAs were detected by human lncRNA microarray in three pairs of PTC and adjacent noncancerous samples. The microarray results revealed that 675 lncRNAs and 751 mRNAs were abnormally expressed in the three PTC samples compared with adjacent noncancerous samples (fold change ≥2.0; P<0.05). To validate the microarray results, 8 differentially expressed lncRNAs were randomly selected for quantitative polymerase chain reaction (qPCR). The results of qPCR were consistent with the microarray data; the 8 lncRNAs had an aberrant expression in the PTC samples compared with the adjacent noncancerous samples. Gene ontology and pathway analysis indicated that there were 7 downregulated pathways and 29 upregulated pathways in PTC. LncRNA classification and subgroup analysis revealed 7 pairs of enhancer-like lncRNA-mRNA, 9 pairs of antisense lncRNA-mRNA and 45 pairs of lncRNA-mRNA were differentially expressed between PTC and their paired noncancerous samples. In conclusion, the present study identified a series of novel PTC-associated lncRNAs. Further study with these lncRNAs is instrumental for the identification of novel target molecules that could lead to improved diagnosis and treatment for PTC.
Interleukin 10(IL-10), as an immunoregulatory cytokine, plays an important role in rheumatoid arthritis (RA). IL-10 gene silencing is associated with the chromatin remodeling in differentiated Th1 and Th2 cells. To explore the relationship between IL-10 promoter methylation and gene silencing in the pathogenesis of RA, IL-10 mRNA, protein expression and promoter methylation status were analyzed in the peripheral blood mononuclear cells (PBMC) of 34 RA patients and 30 healthy controls by reverse transcriptase-polymerase chain reaction (RT-PCR), enzyme-linked immunosorbent assay (ELISA) and methylation specific polymerase chain reaction (MSP), respectively. The results showed that IL-10 mRNA and protein expression in RA patients seemed to be lower than that in healthy controls, but there was no statistically significant difference (P>0.05). IL-10 promoter was methylated at a frequency of 85.29% in RA cases, which was significantly higher than the percentage in healthy controls (43.33%) (c 2 =12.439, P=0.000). IL-10 promoter methylation and mRNA expression showed a strong negative correlation (r=-0.579, P=0.001). IL-10 promoter methylation, but not mRNA expression, also correlated statistically with the number of arthritic joints. However, there were no statistical correlations between IL-10 promoter methylation (or mRNA expression) and clinical indices of RA, such as the levels of erythrocyte sedimentation rate (ESR), C reactive protein (CRP) and rheumatic factor (RF) or age (P>0.05). These findings suggest that promoter methylation may be a crucial mechanism of IL-10 gene inactivation in RA and IL-10 promoter CpG island hypermethylation might be involved in the occurrence and development of RA.
This study aimed to investigate the role and potential mechanism of miR-22 in clear cell ovarian cancer (CCOC) progression. The gene expression profile of GSE16568, including 3 CCOC samples with miR-22 overexpression and 3 negative controls, was downloaded from the Gene Expression Omnibus database. Differentially expressed genes (DEGs) were screened using the limma package in R. Gene Ontology (GO) and pathway enrichment analysis of DEGs were performed by using The Database for Annotation, Visualization and Integrated Discovery (DAVID). Furthermore, protein-protein interaction (PPI) network of the DEGs was constructed using the Search Tool for the Retrieval of Interacting Genes (STRING) database. Besides, the miR-22 -mRNA interaction pairs were predicted to explore the critical genes involved in the cancer. Totally, 95 up-regulated DEGs and 51 down-regulated DEGs were identified. The DEGs were enriched in different GO terms and pathways. The up-regulated genes cyclin-dependent kinases (CDK6), MDM2 oncogene, E3 ubiquitin protein ligase (MDM2), and thrombospondin 1 (THBS1) were involved in the p53 signaling pathway. The up-regulated gene FBJ murine osteosarcoma viral oncogene homolog (FOS) was a hub protein in the PPI network of the DEGs. The down-regulated DEGs including lymphoid enhancer-binding factor 1 (LEF1) and v-myb avian myeloblastosis viral oncogene homolog (MYB) were mainly associated with immunity. Nine DEGs as target genes were identified to be recognized by miR-22. Our study suggested that several key genes such as CDK6, MDM2, LEF1, MYB, and FOS that involved in different pathways including p53 signaling pathway were associated with CCOC progression. miR-22 may play an essential role in cell migration and invasion in CCOC through targeting responsive genes.
Type 2 diabetes mellitus (T2DM) is a complex metabolic disorder caused by the interaction of environmental factors and multiple genes. The genetic background of T2DM is complex and remains to be fully elucidated. MicroRNAs (miRNAs) are negative regulators of gene expression and several miRNAs are associated with the development of T2DM. However, the expression and biological function of miRNA‑9‑3p in lipid metabolism of patients with T2DM remain to be fully elucidated. The predominant aim of the present study was to examine the effect of miRNA‑9‑3p on lipid accumulation in HepG2 cells. To investigate this, an MTT assay was used to determine cell proliferation, and the effects of miRNA‑9‑3p on triglycerides (TG) and total cholesterol (TC) in the HepG2 cells were also examined. Reverse transcription‑quantitative polymerase chain reaction and western blot analyses were used to measure the expression levels of SIRT1 at the gene and protein levels, respectively. The date revealed that downregulation of miRNA‑9‑3p inhibited the proliferation of HepG2 cells, and significantly reduced the accumulation of lipids, and decreased TG and TC content. In addition, the present study demonstrated that inhibition of miRNA‑9‑3p increased the protein expression of sirtuin type 1 (SIRT1), but had no effects on the gene expression of SIRT1. Therefore, these findings demonstrated that the inhibition of miRNA‑9‑3p reduced the proliferation of HepG2 cells and lipid accumulation by upregulating the expression of SIRT1, indicating its potential as a therapeutic target.
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