Tumor progression is the continual selection of variant subpopulations of malignant cells that have acquired increasing levels of genetic instability (Nowell Science 1976, 194, 23-28). This instability is manifested as chromosomal aneuploidy or translocations, viral integration or somatic mutations that typically affect the expression of a gene (oncogene) that is especially damaging to the proper function of a cell. With the recent discovery of non-coding RNAs such as microRNAs (miRNAs), the concept that a target of genetic instability must be a protein-encoding gene is no longer tenable. Over the years, we have conducted several studies comparing the location of miRNA genes to positions of genetic instability, principally retroviral integration sites and chromosomal translocations in the mouse as a means of identifying miRNAs of importance in carcinogenesis. In this current study, we have used the most recent annotation of the mouse miRome (miRBase, release 16.0), and several datasets reporting the sites of integration of different retroviral vectors in a variety of mouse strains and mouse models of cancer, including for the first time a model that shows a propensity to form solid tumors, as a means to further identify or define, candidate oncogenic miRNAs. Several miRNA genes and miRNA gene clusters stand out as interesting new candidate oncogenes due to their close proximity to common retroviral integration sites including miR-29a/b/c and miR106a~363. We also discussed some recently identified miRNAs including miR-1965, miR-1900, miR-1945, miR-1931, miR-1894, and miR-1936 that are close to common retroviral integration sites and are therefore likely to have some role in cell homeostasis.
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http://dx.doi.org/10.3109/15376516.2011.562759 | DOI Listing |
J Biomol Struct Dyn
March 2025
Department of Molecular Medicine, Morsani College of Medicine, University of South Florida, Tampa, FL, USA.
Melanoma, a globally prevalent skin cancer with over 325,000 new cases annually, necessitates a comprehensive under- standing of its molecular components. This study looks at the PRAME (cutaneous melanoma-associated antigen) and BAP1 (gene controlling gene-environment interactions) proteins. Both PRAME and BAP1 are associated with critical genomic alterations that significantly influence melanoma progression and patient outcomes.
View Article and Find Full Text PDFInt J Med Sci
March 2025
Department of Oncology, Third Xiangya Hospital of Central South University, Changsha, 410013, China.
Fucosyltransferase 1 encodes a Golgi membrane protein involved in H-antigen precursor production and plays a critical role in tumor-associated glycosylation and angiogenesis. While FUT1 is known to enhance tumor stemness, adhesion, migration, and drug resistance in specific cancers, its role across diverse cancer types and its association with clinical prognosis and molecular features remain unclear. In this study, FUT1 expression was systematically analyzed across 33 cancer types using data from multiple public databases, including CCLE, TCGA, and GTEx.
View Article and Find Full Text PDFCommun Biol
March 2025
College of Life Sciences, Shaanxi Normal University, Xi'an, 710119, China.
Genomic rearrangements are primary drivers of evolution, promoting biodiversity. Aphids, an agricultural pest with high species diversity, exhibit rapid chromosomal evolution and diverse karyotypes. These variations have been attributed to their unique holocentric chromosomes and parthenogenesis, though this hypothesis has faced scrutiny.
View Article and Find Full Text PDFNat Commun
March 2025
The John Curtin School of Medical Research, The Australian National University, Canberra, Australia.
Missense mutations that disrupt protein structural stability are a common pathogenic mechanism in human genetic disease. Here, we quantify potential disruption of protein stability due to amino acid substitution and show that functionally constrained proteins are less susceptible to large mutational changes in stability. Mechanistically, this relates to greater intrinsic disorder among constrained proteins and to increased B-factors in the ordered regions of constrained proteins.
View Article and Find Full Text PDFMethods Mol Biol
March 2025
The Concern Foundation Laboratories, The Lautenberg Center for Immunology and Cancer Research, Department of Immunology and Cancer Research-IMRIC, Faculty of Medicine, The Hebrew University of Jerusalem, Jerusalem, Israel.
DNA double-strand breaks (DSBs) are a major source of genomic instability. Physiological DSBs are naturally occurring breaks that happen during normal cellular processes. Unlike DNA breaks resulting from DNA damage due to external factors like radiation or chemicals, physiological DSBs play critical roles in various normal biological functions.
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