We previously demonstrated that miR-351-5p regulates nuclear scaffold lamin B1 expression and mediates the anticancer floxuridine-induced necrosis shift to apoptosis in mammalian tumor cells. Notably, it is unknown whether lamin B1 mRNA is a direct target of miR-351-5p. Here, we show that miR-351-5p interacts with a lamin B1 mRNA partial sequence by using the cell-free miRNA and mRNA binding evaluation system. In addition, the interaction of miR-351-5p/lamin B1 mRNA was suppressed by an miR-351-5p inhibitor. Our findings are important in exploring the functions of miRNAs in cellular processes, including cell death.
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http://dx.doi.org/10.1080/15257770.2019.1702675 | DOI Listing |
Biomedicines
November 2024
Department of Ophthalmology, Maisonneuve-Rosemont Hospital Research Center, University of Montréal, Montréal, QC H1T 2M4, Canada.
Choroidal involution is a common feature of age-related ischemic retinopathies such as age-related macular degeneration (AMD). It is now well recognized that endothelial progenitor cells (EPCs) are essential to endothelial repair processes and in maintaining vascular integrity. However, the contribution of EPCs and the role of senescence in age-related choroidal vascular degeneration remain to be investigated.
View Article and Find Full Text PDFMamm Genome
November 2024
Laboratory of Chromatin and Cancer Epigenetics, Department of Biochemistry, All India Institute of Medical Sciences, New Delhi, 110029, India.
Lamins play a crucial role in maintaining nuclear structure and function. Our study investigates the expression patterns and clinical implications of B-type lamins with a special focus on lamin B2 across various cancer types using comprehensive RNA sequencing datasets. We found that high expression levels of lamin B1 and lamin B2 are associated with decreased overall and disease-free survival in cancer.
View Article and Find Full Text PDFAging (Albany NY)
October 2024
Department of Laboratory Medicine and Pathology, University of Washington, Seattle, WA 98195, USA.
Aging Cell
October 2024
Department of Cell Biology and Molecular Genetics, University of Maryland, College Park, Maryland, USA.
Hutchinson-Gilford progeria syndrome (HGPS) is a rare premature aging disorder in children caused by a point mutation in the lamin A gene, resulting in a toxic form of lamin A called progerin. Accelerated atherosclerosis leading to heart attack and stroke are the major causes of death in these patients. Endothelial cell (EC) dysfunction contributes to the pathogenesis of HGPS related cardiovascular diseases (CVD).
View Article and Find Full Text PDFNAR Genom Bioinform
September 2024
Department of Cell Biology and Molecular Genetics, University of Maryland College Park, MD, USA.
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