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OBJECTIVE: To characterize functions of long non-coding RNA (lncRNA) in the progression of epithelial ovarian cancer. PATIENTS AND METHODS: Epithelial ovarian cancer tissues and matching normal tissues were collected from two individual patients for RNA microarray analysis. Besides, twenty-two ovarian cancer samples and ten healthy ovarian epithelial tissues were collected for Reverse Transcription-quantitative Polymerase Chain Reaction (RT-qPCR). Microarray assay suggested that a list of cancer relating mRNAs and lncRNAs were upregulated. The identified lncRNAs were validated via RT-qPCR, which led to the identification of long intergenic non-protein coding RNA 152 (LINC00152). To determine the function of LINC00152 in ovarian cancer, we knocked down the expression of LINC00152 in epithelial ovarian cancer cell line SKOV3 with small interference RNAs (siRNAs). The effects of LIN00152 on the proliferation and cell cycle were determined by comparing the cell viability of SKOV3 cells with LIN00152 knockdown and the control cells with negative siRNA. The cell viability was assessed using Cell Counting Kit-8 (CCK-8) and flow cytometry assay. RNA microarray assay was used again in control and LINC00152 knockdown SKOV3 cells to identify downstream signaling pathways. RESULTS: Fourteen ovarian cancer relating lncRNAs were identified by RNA microarray assay. Up-regulation of LINC00152 was validated via RT-qPCR. A higher expression of LINC00152 in late cancer stage (III-IV) compared to the early stage tumors was also demonstrated. Inhibition of LINC00152 in SKOV3 cells inhibited cell proliferation and induced cell cycle arrest that involved prolonged G1 phase and shortened S phase. The microarray assay data of SKOV3 cells suggested that Cyclin-Dependent Kinase Inhibitor 1C (CDKN1C) was a potential downstream target of LINC00152. CONCLUSIONS: LINC00152 is upregulated in epithelial ovarian cancer tissues comparing to normal tissues. Knockdown of LINC00152 expression inhibits cell proliferation and induces cell cycle arrest. LINC00152 possibly interacts with Tumor Necrosis Factor (TNF) signaling pathway. CDKN1C is a potential downstream target of LINC00152. [ABSTRACT FROM AUTHOR]

OBJECTIVE: To investigate the role of the Notch signaling pathway on the endothelial- mesenchymal transition (EndMT) during vascular endothelial dysfunction and atherosclerosis. MATERIALS AND METHODS: Human coronary artery endothelial cells (HCAEC) were treated with the exogenous Notch homolog 1 (Notch1) factor to activate the Notch1 pathway, and cells were then observed under the microscope for morphologic changes. Changes in the expression of related proteins were detected by Western blot. In vivo experiments were performed using 18 Sprague Dawley® (SD) rats, and GSI factor was used to specifically inhibit Notch pathway activation. Rats were used and randomly divided into three groups: normal diet (ND) group, high-fat diet (HFD) group, and high-fat diet + GSI (HFD+GSI) group, 6 rats in each group. Hematoxylin and eosin (H&E) staining was used to examine the cardiac aortic morphology of the rats in each treatment group. Real- time polymerase chain reaction (RT-PCR) and Western blot were used to detect the expression of Notch1, Hes1, VE-cadherin and α-SMA in the aortic tissues of rats in each group at mRNA and protein levels, respectively. RESULTS: After HCAECs were treated with Notch1, endothelial protein levels of VE-cadherin were significantly decreased and levels of the interstitial protein α-SMA were significantly increased. In the animal model, the rats fed with high-fat diet for two months presented obvious atherosclerosis spots in their aorta, but those fed with the same diet and treated with GSI inhibitor of Notch pathway showed significantly fewer atherosclerosis signs. Compared with ND group, mRNA and protein expression levels of Notch1, Hes1 and α-SMA were significantly increased, and the expression levels of endothelial marker VE-cadherin were significantly decreased in aortas of rats in HFD group. Compared with the rats in HFD group, the rats in HFD+ GSI group showed significantly reduced expression levels of Notch1, Hes1 and α-SMA. CONCLUSIONS: The activation of Notch signaling pathway can induce the EndMT progression and promote the development of atherosclerotic lesions. [ABSTRACT FROM AUTHOR]