Previous studies have shown that microRNA-186 (miR-186) is overexpressed in various human cancers and is associated with the regulation of the carcinogenic processes. However, the underlying mechanisms of this microRNA in melanoma remain largely unknown. In the present study, the overexpression of miR-186 was identified in melanoma tissues and melanoma cells compared to the expression of miR-186 in the matched tumor adjacent tissues and normal human epidermal melanocytes. Overexpression of miR-186 promoted the proliferation and anchorage-independent growth of melanoma cells, whereas inhibition of miR-186 reduced this effect. Bioinformatics analysis also revealed cylindromatosis (CYLD), a putative tumor suppressor, to be a potential target of miR-186. Luciferase reporter assays showed that miR-186 directly targeted the 3'-untranslated regions of CYLD messenger RNA. Additional experiments showed that overexpression of miR-186 promoted the proliferation of melanoma cells, which was consistent with the inhibitory effects induced by knockdown of CYLD. In summary, the present study indicated that miRNA-186 plays a crucial role in melanoma growth and its oncogenic effect is mediated chiefly through the direct suppression of CYLD expression.
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http://dx.doi.org/10.3892/ol.2016.5002 | DOI Listing |
Toxicol Appl Pharmacol
December 2024
Department of Pharmacology and Toxicology, University of Louisville, 505 S. Hancock Street, Louisville, KY 40202, USA; Center for Integrative Environmental Health Sciences, University of Louisville, 505 S. Hancock Street, Louisville, KY 40202, USA. Electronic address:
Dysregulated miRNA expression contributes to development of arsenic-induced cutaneous squamous cell carcinoma (cSCC). hsa-miR-186 (miR-186) is overexpressed in arsenical cSCC tissues as well as in preclinical cell line model of arsenical cSCC. Simultaneous miR-186 overexpression and chronic inorganic trivalent arsenite (iAs; 100 nM) exposure transformed human HaCaT cell line preferentially over miR-186 overexpression or iAs exposure alone.
View Article and Find Full Text PDFExpert Rev Clin Immunol
October 2024
Pediatric Laboratory, Hunan Provincial People's Hospital (The First Hospital Affiliated with Hunan Normal University), Changsha, Hunan, China.
Objective: To probe the involvement of long noncoding RNA zinc finger antisense 1 (ZFAS1)/microRNA (miR)-186-5p axis in inhibiting oxidative stress in myocardial ischemia-reperfusion injury (MIRI) by targeting B-cell translocation gene 2 (BTG2).
Methods: The MIRI mice model was established by ligating the left anterior descending branch of the left coronary artery in C57BL/6 mice. The in vitro MIRI model was constructed by hypoxia and reoxygenation of HL-1 cardiomyocytes.
Mol Psychiatry
September 2024
CNC-Centre for Neuroscience and Cell Biology, University of Coimbra, 3004-504, Coimbra, Portugal.
J Exp Clin Cancer Res
August 2024
Guangzhou Key Laboratory of Digestive Diseases, Guangzhou Digestive Disease Center, Guangzhou First People's Hospital, School of Medicine, South China University of Technology, Guangzhou, Guangdong, 510180, China.
Background: Long non-coding RNAs (LncRNAs) have been implicated as critical regulators of cancer tumorigenesis and progression. However, their functions and molecular mechanisms in colorectal cancer (CRC) still remain to be further elucidated.
Methods: LINC00460 was identified by differential analysis between human CRC and normal tissues and verified by in situ hybridization (ISH) and qRT-PCR.
Epigenetics
December 2024
Department of Pulmonary Medicine, The Affiliated Cancer Hospital of Xinjiang Medical University, Urumqi, Xinjiang, China.
Lung cancer is one familiar cancer that threatens the lives of humans. circCTNNB1 has been disclosed to have regulatory functions in some diseases. However, the functions and related regulatory mechanisms of circCTNNB1 in lung cancer remain largely indistinct.
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