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Long non-coding RNAs (lncRNAs), some of the most abundant epigenetic regulators, play an important role in esophageal squamous cell carcinoma (ESCC). In the current study, the functions and mechanisms of the lncRNA LINC00673 were investigated. The expression levels of LINC00673 and its potential target genes were assessed by quantitative real-time polymerase chain reaction (qPCR) in ESCC surgical specimens and ESCC cell lines. RNA fluorescence in situ hybridization (RNA FISH) was employed to detect the subcellular location and the levels of LINC00673 in ESCC samples from patients with different survival times. LINC00673 function in ESCC carcinogenesis was also evaluated in vivo and in vitro. Cell cycle synchronization was performed using serum withdrawal; the cell cycle was monitored by fluorescence analysis and cellular DNA was detected by flow cytometry. The molecular mechanisms underlying LINC00673 were explored via Western blotting, chromatin immunoprecipitation (ChIP), and ChIP-PCR. Up-regulated LINC00673 was associated with poor prognosis in ESCC patients and promoted the proliferation of ESCC cells both in vitro and in vivo. Compared to the control group, depletion of LINC00673 in ESCC cells arrested the cell cycle, at least, at the G1/S checkpoint. Knockdown of LINC00673 significantly enhanced posttranscriptional expression of CDKN2C, and histone 3 lysine 27 trimethylation (H3K27me3) was enriched at the promoter region of CDKN2C. After inhibiting EZH2, the CDKN2C expression levels were increased. The present findings are the first to reveal that LINC00673 represses CDKN2C expression and promotes ESCC cell proliferation by elevating EZH2-mediated H3K27me3 levels. These data suggest that LINC00673 regulates the cell cycle in ESCC and that it is a promising target for clinical therapy. [ABSTRACT FROM AUTHOR]

miRNAs are increasingly being implicated as key regulators of cell proliferation, apoptosis, and differentiation. miRNA-34c appears to play a crucial role in cancer pathogenesis wherein it exerts its effect as a tumor suppressor. However, the role of miR-34c in myoblast proliferation remains poorly understood. Here, we found that overexpression miR-34c inhibited myoblasts proliferation by reducing the protein and mRNA expression of cell cycle genes. In contrast, blocking the function of miR-34c promoted myoblasts proliferation and increased the protein and mRNA expression of cell cycle genes. Moreover, miR-34c directly targeted YY1 and inhibited its expression. Similar to overexpression miR-34c, knockdown of YY1 by siRNA suppressed myoblasts proliferation. Our study provides novel evidence for a role of miR-34c in inhibiting myoblasts proliferation by repressing YY1. Thus, miR-34c has the potential to be used to enhance skeletal muscle development and regeneration. [ABSTRACT FROM PUBLISHER]

Purpose. We examined the role of miR-20b in development of thymoma-associated myasthenia gravis, especially in T cell proliferation and activation. Materials and Methods. Using qRT-PCR, we assessed expression levels of miR-20b and its target genes in cultured cells and patient samples and examined the proliferation of cultured cells, using MTT cell proliferation assays and flow cytometry based cell cycle analysis. Activation of T cells was determined by both flow cytometry and qRT-PCR of activation-specific marker genes. Results. Expression of miR-20b was downregulated in samples of thymoma tissues and serum from patients with thymoma-associated myasthenia gravis. In addition, T cell proliferation and activation were inhibited by ectopic overexpression of miR-20b, which led to increased T cell proliferation and activation. NFAT5 and CAMTA1 were identified as targets of miR-20b. Expression levels of NFAT5 and CAMTA1 were inhibited by miR-20b expression in cultured cells, and the expression levels of miR-20b and NFAT5/CAMTA1 were inversely correlated in patients with thymoma-associated myasthenia gravis. Conclusion. miR-20b acts as a tumor suppressor in the development of thymoma and thymoma-associated myasthenia gravis. The tumor suppressive function of miR-20b in thymoma could be due to its inhibition of NFAT signaling by repression of NFAT5 and CAMTA1 expression. [ABSTRACT FROM AUTHOR]