Glioma is the most common type of primary tumor of the central nervous system. The present study aimed to demonstrate the role of miR-101 and cyclooxygenase-2 (COX-2) in the initiation and development of glioma. The expression of miR-101 and COX-2 in normal and malignant human glial cells and tissues was determined by western blotting and quantitative polymerase chain reaction analysis. The role of miR-101 on COX-2 expression was evaluated by a dual-luciferase reporter assay. The effects of miR-101 and COX-2 in glioma cell proliferation and invasion was verified by CCK-8 test and Transwell assays, respectively. The present study demonstrated that miR-101 expression was downregulated while COX-2 was upregulated in glioma tissues and cells. Furthermore, transfection of miR-101 significantly downregulated COX-2 expression in both U373 and U87 glioma cells. In addition, further experiments revealed that overexpression of miR-101 resulted in significant inhibition of the proliferation and migration of glioma cells, and the growth of established tumors. Direct downregulation of COX-2 by transfection with corresponding small interfering RNA also inhibited the proliferation and invasion of glioma cells. These results indicate that downregulation of miR-101 is involved in the initiation and development of glioma via COX-2 upregulation.
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http://dx.doi.org/10.3892/ol.2016.4939 | DOI Listing |
Clin Biochem
September 2022
Department of Medical Biochemistry, Cerrahpasa Faculty of Medicine, Istanbul University-Cerrahpasa, Istanbul, Turkey; Department of Medical Biochemistry, Faculty of Medicine, İstanbul Atlas University, Istanbul, Turkey. Electronic address:
Background: Pulmonary arterial hypertension (PAH) is a rare disease with a poor prognosis. The suppression of cyclooxygenase-2 (COX-2) expression has been known to impair vascular function in endothelial cells; however, the epigenetic factors that cause this are largely obscure. Our aim in this study was to examine the polymorphisms in the gene for COX-2 (PTGS2) and related miRNAs regulating its level in a single-center cohort of patients with PAH.
View Article and Find Full Text PDFBreast Cancer Res Treat
June 2021
Sharjah Institute for Medical Research, University of Sharjah, 27272, Sharjah, United Arab Emirates.
Purpose: Extravasation of triple-negative (TN) metastatic breast cancer (BC) cells through the brain endothelium (BE) is a critical step in brain metastasis (BM). During extravasation, metastatic cells induce alteration in the inter-endothelial junctions and transmigrate through the endothelial barrier. Transmigration of metastatic cells is mediated by the upregulation of cyclooxygenase-2 (COX-2) that induces matrix metalloproteinase-1 (MMP-1) capable of degrading inter-endothelial junctional proteins.
View Article and Find Full Text PDFBiochem Pharmacol
July 2021
State Key Laboratory of Molecular Vaccinology and Molecular Diagnostics, School of Public Health, Xiamen University, Xiamen 361102, China. Electronic address:
Exposure to toxic metal contaminants, such as cadmium compounds (Cd), has been shown to induce adverse effects on various organs and tissues. In particular, blood vessels are severely impacted by Cd exposure, which may lead to cardiovascular diseases (CVDs). According to previous studies, CVDs are associated with increased cyclooxygenase 2 (COX-2) levels.
View Article and Find Full Text PDFPharmaceuticals (Basel)
July 2020
Sharjah Institute for Medical Research, University of Sharjah, Sharjah P.O. Box 27272, UAE.
Brain metastases represent one of the incurable end stages in breast cancer (BC). Developing effective or preventive treatments is hampered by a lack of knowledge on the molecular mechanisms driving brain metastasis. Transmigration of BC cells through the brain endothelium is a key event in the pathogenesis of brain metastasis.
View Article and Find Full Text PDFBiochem Biophys Res Commun
November 2018
Gongli Hospital of Pudong District, Shanghai, PR China. Electronic address:
Background: Nasopharyngeal carcinoma (NPC) is the most common type of head and neck cancers which is notable for its distinctive pattern of geographical distribution. HOTAIR has been reported to regulate nasopharyngeal carcinoma tumorigenesis and progression. However, the detailed mechanism underlying HOTAIR-promoted nasopharyngeal carcinoma remains not fully understood.
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