125 research outputs found

    Metabolic Inhibitor Effects on Eyespot Formation in Regenerating Planaria

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    Planaria are flatworms known for their remarkable ability to regenerate. Glycolytic activity has been shown to increase during planarian regeneration (Osuma et al., 2017) and regeneration requires both an increase in mitotic activity and an increase in apoptotic activity to successfully regrow missing structures (Pellettieri et al., 2010; Wenemoser & Reddien, 2010). The objectives of this study are to determine if metabolic inhibitors affect the time needed to regenerate eyespots after head amputation as a measurement of regeneration and if there are any correlations between average numbers of mitotic and apoptotic cells in regenerating planaria in the presence or absence of metabolic inhibitors. Planaria (D. dorotocephala and D. tigrina) were exposed to non-lethal doses of metabolic inhibitors after amputation between the head and the pharynx to determine if metabolic inhibitors affect eyespot regeneration times. Mucus removal, fixation, and bleaching were used to prepare planaria for immunolabeling procedures. Mitotic cells were labeled to determine if metabolic inhibitors affect average numbers of mitotic cells in regenerating planaria. Immunolabelling procedures were used in an attempt to visualize apoptotic cells in planaria. Results from the exposure experiments suggest that the earlier planaria are exposed to metabolic inhibitors after amputation, the longer it takes to regrow eyespots. By comparing the average number of mitotic cells planaria in the presence or absence of metabolic inhibitors, it was determined that delays in eyespot formation are not associated with changes in the average number of mitotic cells. Further studies should be conducted to test for significant differences between apoptotic cells in inhibitor-treated and untreated planaria

    Mechanisms and role of microRNA deregulation in cancer onset and progression

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    MicroRNAs are key regulators of various fundamental biological processes and, although representing only a small portion of the genome, they regulate a much larger population of target genes. Mature microRNAs (miRNAs) are single-stranded RNA molecules of 20–23 nucleotide (nt) length that control gene expression in many cellular processes. These molecules typically reduce the stability of mRNAs, including those of genes that mediate processes in tumorigenesis, such as inflammation, cell cycle regulation, stress response, differentiation, apoptosis and invasion. MicroRNA targeting is mostly achieved through specific base-pairing interactions between the 5′ end (‘seed’ region) of the miRNA and sites within coding and untranslated regions (UTRs) of mRNAs; target sites in the 3′ UTR diminish mRNA stability. Since miRNAs frequently target hundreds of mRNAs, miRNA regulatory pathways are complex. Calin and Croce were the first to demonstrate a connection between microRNAs and increased risk of developing cancer, and meanwhile the role of microRNAs in carcinogenesis has definitively been evidenced. It needs to be considered that the complex mechanism of gene regulation by microRNAs is profoundly influenced by variation in gene sequence (polymorphisms) of the target sites. Thus, individual variability could cause patients to present differential risks regarding several diseases. Aiming to provide a critical overview of miRNA dysregulation in cancer, this article reviews the growing number of studies that have shown the importance of these small molecules and how these microRNAs can affect or be affected by genetic and epigenetic mechanisms
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