Тип публикации: статья из журнала
Год издания: 2019
Идентификатор DOI: 10.1016/j.jid.2019.07.549
Аннотация: microRNAs are considered as a class of epigenetic regulators that results in translational repression or decay of target mRNAs. Each microRNA may have up to several hundred mRNA targets, and several genes may be regulated by one unique microRNA. Therefore microRNAs are involved in numerous pathological conditions regulation includiПоказать полностьюng carcinogenesis. MiR-204-5p was revealed as one of the most down-regulated microRNAs in melanoma versus melanocytic nevi according to our microarray studies. Functional analysis of melanoma cells was performed and included gain and loss of function experiments followed by melanoma cells proliferation, apoptosis, migration, invasion, colony formation evaluation. We revealed that miR-204-5p mimic application induced an increase of BRO, SK-MEL-1 melanoma cells proliferation whereas miR-204-5p inhibitor diminished the proliferation in these cells. Besides, miR-204-5p inhibitor stimulated melanoma cells migration. To further investigate miR-204-5p functioning in melanoma we used B16-melanoma bearing mice model where mmu-miR-204-5p miRCURY LNA™ was applied. We found out the decrease of Ki-67-positive melanoma cells in the tumor although tumor mass and tumor volume alterations were not determined in specific miR-204-5p inhibitor treated animals group versus control group. Tumor lymphocyte infiltration was not changed whereas we observed the diminished number of CD45R0 cells in lungs and liver. Toxicity studies revealed no changes in body weight, ALT, AST serum levels, miR-122 and GAPDH levels in the liver under miR-204-5p inhibitor treatment in vivo. Taking together, these findings show that miR-204-5p levels modulation may have impact on melanoma progression. In addition, miR-204-5p inhibitor application did not show significant toxic effect in vivo.
Журнал: Journal of Investigative Dermatology
Выпуск журнала: Т.139, №S9
Номера страниц: 300
ISSN журнала: 0022202X
Издатель: John Wiley & Sons, Incorporated