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lncRNA SNHG14 promotes the proliferation, migration, and invasion of thyroid tumour cells by regulating miR-93-5p
- Fang Tian, Huimin Ying, Shuaiju Liao, Yuanyuan Wang, Quansheng Wang
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Long non-coding RNAs (lncRNAs) exert vital functions in the occurrence and development of various tumours. The aim of this study was to examine the regulatory effect and underlying molecular mechanism of lncRNA small nucleolar RNA host gene 14 (SNHG14) on the proliferation, invasion and migration of thyroid tumour cells. The expression of SNHG14 in thyroid tumour cell lines was determined using qRT-PCR. CCK-8 and western blot were used to detect the effects of SNHG14 on proliferation and apoptosis of thyroid tumour cells. The effect of SNHG14 on the migration and invasion of thyroid tumour cells was analyzed using immunofluorescence, wound-healing and transwell assays. A targeting relationship between SNHG14 and miR-93-5p was determined using bioinformatics software and luciferase reporter assays. In addition, CCK-8, immunofluorescence, wound-healing and transwell assays were applied to demonstrate that SNHG14 promoted the proliferation, migration and invasion of thyroid tumour cells by targeting miR-93-5p. The biological function of SNHG14 in vivo was explored through a xenograft model and immunohistochemistry. SNHG14 was upregulated in thyroid tumour cells compared with normal cells. Downregulation of SNHG14 effectively reduced the proliferation, migration and invasion of TPC-1 cells, and induced cell apoptosis. Moreover, SNHG14 directly targeted miR-93-5p and there was a negative correlation between them. Further functional experiments illustrated that miR-93-5p overexpression dramatically reversed the promoting role of SNHG14 in proliferation, migration and invasion of TPC-1 cells. Our results demonstrated that SNHG14 promotes the proliferation, invasion and migration of thyroid tumour cells by downregulating miR-93-5p.
94 - Genetics of Coronary Artery Disease and Myocardial Infarction: The MEF2 Signaling Pathway in the Endothelium
- from PART II - ENDOTHELIAL CELL AS INPUT-OUTPUT DEVICE
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- By Stephen R. Archacki, Lerner Research Institute and Center for Cardiovascular Genetics, Cleveland Clinic Foundation; of Molecular Medicine, Cleveland Clinic Lerner College of Medicine of Case Western Reserve University, Cleveland State University, Ohio, Sun-Ah You, Lerner Research Institute and Center for Cardiovascular Genetics, Cleveland Clinic Foundation; of Molecular Medicine, Cleveland Clinic Lerner College of Medicine of Case Western Reserve University, Quansheng Xi, Lerner Research Institute and Center for Cardiovascular Genetics, Cleveland Clinic Foundation; of Molecular Medicine, Cleveland Clinic Lerner College of Medicine of Case Western Reserve University, Qing Wang, Lerner Research Institute and Center for Cardiovascular Genetics, Cleveland Clinic Foundation; of Molecular Medicine, Cleveland Clinic Lerner College of Medicine of Case Western Reserve University, Cleveland State University, Ohio
- Edited by William C. Aird, Harvard University, Massachusetts
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- Book:
- Endothelial Biomedicine
- Published online:
- 04 May 2010
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- 03 September 2007, pp 847-854
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Summary
Coronary artery disease (CAD) is the leading cause of death and disability in the United States and other developed countries (1). CAD is characterized by the formation of atherosclerotic plaques in the walls of the coronary arteries (2–5). The structure of a normal coronary artery consists of the endothelium (a single layer of endothelial cells [ECs]) on the luminal side; followed by the intima, consisting of collagens and proteoglycans; the middle layer (media) of smooth muscle cells (SMCs); and the outside layer (adventitia), consisting of connective tissues, fibroblasts, and more SMCs (Figure 94.1). Development of CAD starts with binding of blood monocytes to the endothelium through cell adhesion molecules including vascular cell adhesion molecule (VCAM)-1 and intercellular adhesion molecule (ICAM)-1, followed by infiltration of lipoproteins and monocytes into the media region, which attract oxidized lipids and form foam cells, the hallmark of an arterial lesion. Necrosis and apoptosis of foam cells lead to a necrotic core with a mass of cell debris and lipids. Macrophages and the foam cells secrete cytokines, inflammatory molecules, and growth factors that induce SMC migration, proliferation, and the production of extra cellular matrix-forming plaques with fibrous caps. When the plaques are stable, the patient may not experience any symptoms of chest pain. However, plaque rupture may lead to thrombosis and secondary unstable angina, acute myocardial infarction (MI), or sudden death (6, 7).
This overview of the pathophysiology of CAD and MI represents the current prevailing mechanism for the pathogenesis of CAD and MI and suggests that CAD is an inflammatory process affecting the endothelium (i.e., endothelial dysfunction) in addition to a disease of lipid metabolism, SMC proliferation and migration, and up regulation of immune responses.